The term “total peripheral vascular resistance” refers to the total resistance of the arterioles. However, changes in tone in various departments cordially vascular system are different. In some vascular areas there may be pronounced vasoconstriction, in others - vasodilation. However, OPSS is important for differential diagnosis type of hemodynamic disorders.

In order to imagine the importance of TPR in the regulation of MOS, it is necessary to consider two extreme options - an infinitely large TPR and the absence of it in the blood flow. With a large peripheral vascular resistance, blood cannot flow through the vascular system. Under these conditions, even with good heart function, blood flow stops. In some pathological conditions, blood flow in tissues decreases as a result of an increase in peripheral vascular resistance. A progressive increase in the latter leads to a decrease in MOC. With zero resistance, blood could flow freely from the aorta into the vena cava and then into the right heart. As a result, the pressure in the right atrium would become equal to the pressure in the aorta, which would greatly facilitate the release of blood into the arterial system, and the MOS would increase 5-6 times or more. However, in a living organism, OPSS can never become equal to 0, just as it can never become infinitely large. In some cases, peripheral vascular resistance decreases (liver cirrhosis, septic shock). When it increases by 3 times, MVR can decrease by half at the same pressure values ​​in the right atrium.

Division of vessels according to their functional significance. All vessels of the body can be divided into two groups: resistance vessels and capacitive vessels. The former regulate the value of peripheral vascular resistance, blood pressure and the degree of blood supply to individual organs and systems of the body; the latter, due to their large capacity, are involved in maintaining venous return to the heart, and consequently, MOS.

The vessels of the “compression chamber” - the aorta and its large branches - maintain a pressure gradient due to distensibility during systole. This softens the pulsatile release and makes the flow of blood to the periphery more uniform. Precapillary resistance vessels - small arterioles and arteries - maintain hydrostatic pressure in the capillaries and tissue blood flow. They account for most of the resistance to blood flow. Precapillary sphincters, changing the number of functioning capillaries, change the exchange surface area. They contain a-receptors, which, when exposed to catecholamines, cause spasm of the sphincters, impaired blood flow and cell hypoxia. α-blockers are pharmacological agents, reducing irritation of a-receptors and relieving spasm in the sphincters.

Capillaries are the most important vessels exchange. They carry out the process of diffusion and filtration - absorption. Solutes pass through their wall in both directions. They belong to the system of capacitive vessels and in pathological conditions can accommodate up to 90% of the blood volume. Under normal conditions, they contain up to 5-7% blood.

Post-capillary resistance vessels - small veins and venules - regulate hydrostatic pressure in the capillaries, resulting in the transport of the liquid part of the blood and interstitial fluid. The humoral factor is the main regulator of microcirculation, but neurogenic stimuli also have an effect on the pre- and postcapillary sphincters.

Venous vessels, containing up to 85% of the blood volume, do not play a significant role in resistance, but act as a container and are most susceptible to sympathetic influences. General cooling, hyperadrenalineemia and hyperventilation lead to venous spasm, which is of great importance in the distribution of blood volume. Changing the capacity of the venous bed regulates the venous return of blood to the heart.

Shunt vessels - arteriovenous anastomoses - in internal organs They function only in pathological conditions; they perform a thermoregulatory function in the skin.

8) classification of blood vessels.

Blood vessels- elastic tubular formations in the body of animals and humans, through which the force of a rhythmically contracting heart or a pulsating vessel carries out the movement of blood throughout the body: to organs and tissues through arteries, arterioles, arterial capillaries, and from them to the heart - through venous capillaries, venules and veins .

Among the vessels of the circulatory system there are arteries, arterioles, capillaries, venules, veins And arteriole-venous anastomoses; The vessels of the microcirculatory system mediate the relationship between arteries and veins. Vessels of different types differ not only in their thickness, but also in tissue composition and functional features.

Arteries are vessels through which blood moves away from the heart. Arteries have thick walls, which contain muscle fibers, as well as collagen and elastic fibers. They are very elastic and can contract or expand, depending on the amount of blood pumped by the heart.

Arterioles are small arteries that immediately precede capillaries in the blood flow. Smooth muscle fibers predominate in their vascular wall, thanks to which arterioles can change the size of their lumen and, thus, resistance.

Capillaries are tiny blood vessels, so thin that substances can freely penetrate their walls. Through the capillary wall, nutrients and oxygen are released from the blood into cells and carbon dioxide and other waste products are transferred from cells to the blood.

Venules are small blood vessels that provide big circle outflow of oxygen-depleted blood saturated with waste products from the capillaries into the veins.

Veins are vessels through which blood moves to the heart. The walls of veins are less thick than the walls of arteries and contain correspondingly fewer muscle fibers and elastic elements.

9) Volumetric blood flow velocity

The volumetric flow rate of the blood (blood flow) of the heart is a dynamic indicator of the activity of the heart. The variable corresponding to this indicator physical quantity characterizes the volumetric amount of blood passing through the cross-section of the flow (in the heart) per unit time. The volumetric blood flow velocity of the heart is estimated using the formula:

CO = HR · SV / 1000,

Where: HR- heart rate (1/ min), SV- systolic blood flow volume ( ml, l). The circulatory system, or cardiovascular system, is a closed system (see diagram 1, diagram 2, diagram 3). It consists of two pumps (right heart and left heart), connected in series by blood vessels of the systemic circulation and blood vessels of the pulmonary circulation (vessels of the lungs). In any aggregate cross section of this system, the same amount of blood flows. In particular, under the same conditions, the flow of blood flowing through the right heart is equal to the flow of blood flowing through the left heart. In a person at rest, the volumetric velocity of blood flow (both right and left) of the heart is ~4.5 ÷ 5.0 l / min. The purpose of the circulatory system is to ensure continuous blood flow to all organs and tissues in accordance with the needs of the body. The heart is a pump that pumps blood through the circulatory system. Together with the blood vessels, the heart actualizes the purpose of the circulatory system. Hence, the volumetric blood flow velocity of the heart is a variable that characterizes the efficiency of the heart. Heart blood flow is controlled by the cardiovascular center and is influenced by a number of variables. The main ones are: the volumetric flow rate of venous blood to the heart ( l / min), end-diastolic blood flow volume ( ml), systolic blood flow volume ( ml), end-systolic blood flow volume ( ml), heart rate (1/ min).

10) Linear speed of blood flow (blood flow) is a physical quantity that is a measure of the movement of blood particles that make up the flow. Theoretically, it is equal to the distance traveled by a particle of the substance that makes up the flow per unit time: v = L / t. Here L- path ( m), t- time ( c). In addition to the linear velocity of blood flow, there is a distinction between the volumetric velocity of blood flow, or volumetric blood flow velocity. Average linear velocity of laminar blood flow ( v) is estimated by integrating the linear velocities of all cylindrical flow layers:

v = (dP r 4 ) / (8η · l ),

Where: dP- difference in blood pressure at the beginning and end of a section of a blood vessel, r- radius of the vessel, η - blood viscosity, l - length of the vessel section, coefficient 8 - this is the result of integrating the velocities of the blood layers moving in the vessel. Volumetric blood flow velocity ( Q) And linear speed blood flow are related by the relationship:

Q = vπ r 2 .

Substituting into this relation the expression for v we obtain the Hagen-Poiseuille equation (“law”) for the volumetric blood flow rate:

Q = dP · (π r 4 / 8η · l ) (1).

Based on simple logic, it can be argued that the volumetric velocity of any flow is directly proportional to the driving force and inversely proportional to the resistance to flow. Similarly, the volumetric velocity of blood flow ( Q) is directly proportional to the driving force (pressure gradient, dP), providing blood flow, and is inversely proportional to the resistance to blood flow ( R): Q = dP / R. From here R = dP / Q. Substituting expression (1) into this relation for Q, we obtain a formula for estimating blood flow resistance:

R = (8η · l ) / (π r 4 ).

From all these formulas it is clear that the most significant variable that determines the linear and volumetric velocity of blood flow is the lumen (radius) of the vessel. This variable is the main variable in controlling blood flow.

Vascular resistance

Hydrodynamic resistance is directly proportional to the length of the vessel and blood viscosity and inversely proportional to the radius of the vessel to the 4th power, that is, it most depends on the lumen of the vessel. Since arterioles have the greatest resistance, peripheral vascular resistance depends mainly on their tone.

There are central mechanisms for regulating arteriolar tone and local mechanisms for regulating arteriolar tone.

The first includes nervous and hormonal influences, the second - myogenic, metabolic and endothelial regulation.

Sympathetic nerves have a constant tonic vasoconstrictor effect on the arterioles. The magnitude of this sympathetic tone depends on the impulse received from the baroreceptors of the carotid sinus, aortic arch and pulmonary arteries.

The main hormones normally involved in the regulation of arteriolar tone are adrenaline and norepinephrine, produced by the adrenal medulla.

Myogenic regulation is reduced to contraction or relaxation of vascular smooth muscle in response to changes in transmural pressure; at the same time, the tension in their wall remains constant. This ensures autoregulation of local blood flow - constancy of blood flow under changing perfusion pressure.

Metabolic regulation ensures vasodilation with an increase in basal metabolism (due to the release of adenosine and prostaglandins) and hypoxia (also due to the release of prostaglandins).

Finally, endothelial cells release a number of vasoactive substances - nitric oxide, eicosanoids (arachidonic acid derivatives), vasoconstrictor peptides (endothelin-1, angiotensin II) and oxygen free radicals.

12) blood pressure in different parts of the vascular bed

Blood pressure in various parts of the vascular system. The average pressure in the aorta is maintained at a high level (approximately 100 mmHg) as the heart continually pumps blood into the aorta. On the other side, arterial pressure varies from a systolic level of 120 mm Hg. Art. up to a diastolic level of 80 mm Hg. Art., since the heart pumps blood into the aorta periodically, only during systole. As blood moves through the systemic circulation, the average pressure steadily decreases, and at the point where the vena cava enters the right atrium it is 0 mm Hg. Art. The pressure in the capillaries of the systemic circulation decreases from 35 mm Hg. Art. at the arterial end of the capillary up to 10 mm Hg. Art. at the venous end of the capillary. The average “functional” pressure in most capillary networks is 17 mmHg. Art. This pressure is sufficient to force a small amount of plasma through small pores in the capillary wall, while nutrients easily diffuse through these pores to the cells of nearby tissues. The right side of the figure shows the change in pressure in different parts of the pulmonary (pulmonary) circulation. In the pulmonary arteries, pulse pressure changes are visible, as in the aorta, but the pressure level is much lower: systolic pressure in pulmonary artery- on average 25 mm Hg. Art., and diastolic - 8 mm Hg. Art. Thus, the average pulmonary artery pressure is only 16 mmHg. Art., and the average pressure in the pulmonary capillaries is approximately 7 mm Hg. Art. At the same time, the total volume of blood passing through the lungs per minute is the same as in the systemic circulation. Low pressure in the pulmonary capillary system is necessary for the gas exchange function of the lungs.

Owners of patent RU 2481785:

The group of inventions relates to medicine and can be used in clinical physiology, physical education and sports, cardiology, and other areas of medicine. In healthy subjects, heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) are measured. Determines the proportionality coefficient K depending on body weight and height. Calculate the value of OPSS in Pa·ml -1 ·s using the original mathematical formula. Then the minute blood volume (MBV) is calculated using a mathematical formula. The group of inventions makes it possible to obtain more exact values OPSS and IOC, assess the state of central hemodynamics through the use of physically and physiologically based calculation formulas. 2 n.p.f-ly, 1 pr.

The invention relates to medicine, in particular to the determination of indicators reflecting the functional state of the cardiovascular system, and can be used in clinical physiology, physical culture and sports, cardiology, and other areas of medicine. For most physiological studies conducted on humans, in which pulse, systolic (SBP) and diastolic (DBP) blood pressure are measured, integral indicators of the state of the cardiovascular system are useful. The most important of these indicators, reflecting not only the functioning of the cardiovascular system, but also the level of metabolic and energy processes in the body, is the minute blood volume (MBV). Total peripheral vascular resistance (TPVR) is also the most important parameter used to assess the state of central hemodynamics.

The most popular method for calculating stroke volume (SV), and based on it the IOC, is Starr’s formula:

VR=90.97+0.54 PD-0.57 DBP-0.61 V,

where PP is pulse pressure, DBP is diastolic pressure, B is age. Next, the IOC is calculated as the product of SV and heart rate (IOC = SV·HR). But the accuracy of Starr's formula has been questioned. The correlation coefficient between the SV values ​​obtained by impedance cardiography methods and the values ​​calculated using the Starr formula was only 0.288. According to our data, the discrepancy between the value of SV (and, consequently, IOC), determined using the tetrapolar rheography method and calculated using the Starr formula, in some cases exceeds 50%, even in a group of healthy subjects.

There is a known method for calculating the IOC using the Lilje-Strander and Zander formula:

IOC=AD ed. · Heart rate,

where is AD ed. - reduced blood pressure, blood pressure ed. = PP·100/Avg.Da, HR is heart rate, PP is pulse pressure, calculated by the formula PP=SBP-DBP, and Avg.Da is the average pressure in the aorta, calculated by the formula: Avg.Da=(SBP+ DBP)/2. But in order for the Lilje-Strander and Zander formula to reflect the IOC, it is necessary that the numerical value of AD ed. , which is PP multiplied by a correction factor (100/Sr.Da), coincided with the value of stroke ejected by the ventricle of the heart during one systole. In fact, with a value of Av.Da = 100 mm Hg. blood pressure value ed. (and, consequently, SV) is equal to the value of PD, with Average Yes<100 мм рт.ст. - АД ред. несколько превышает ПД, а при Ср.Да>100 mmHg - AD ed. becomes less than PD. In fact, the value of PD cannot be equated to the value of SV even with Average Da=100 mmHg. Normal average values ​​of PP are 40 mm Hg, and SV are 60-80 ml. A comparison of the IOC values ​​calculated using the Lilje-Strander and Zander formula in a group of healthy subjects (2.3-4.2 l) with the normal IOC values ​​(5-6 l) shows a discrepancy between them of 40-50%.

The technical result of the proposed method is to increase the accuracy of determining minute blood volume (MBV) and total peripheral vascular resistance (TPVR) - the most important indicators, reflecting the work of the cardiovascular system, the level of metabolic and energy processes in the body, assessing the state of central hemodynamics through the use of physically and physiologically based calculation formulas.

A method is claimed for determining integral indicators of the state of the cardiovascular system, which consists in measuring the subject's heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), weight and height at rest. After this, total peripheral vascular resistance (TPVR) is determined. The value of TPSS is proportional to diastolic blood pressure (DBP) - the higher the DBP, the greater the TPSS; time intervals between periods of ejection (Tpi) of blood from the ventricles of the heart - the longer the interval between periods of ejection, the greater the TPR; circulating blood volume (CBV) - the more BCC, the lower the OPSS (CBV depends on a person’s weight, height and gender). OPSS is calculated using the formula:

OPSS=K·DAD·(Tsts-Tpi)/Tpi,

where DBP is diastolic blood pressure;

Tsk - period cardiac cycle, calculated by the formula Tstc=60/HR;

Tpi is the expulsion period, calculated by the formula:

Tpi=0.268·Tsc 0.36 ≈Tsc·0.109+0.159;

K is a proportionality coefficient depending on body weight (BW), height (P) and gender of a person. K=1 in women with MT=49 kg and P=150 cm; in men with MT=59 kg and P=160 cm. In other cases, K for healthy subjects is calculated according to the rules presented in Table 1.

MOK=Avg.Da·133.32·60/OPSS,

Avg.Yes=(GARDEN+DBP)/2;

Table 2 shows examples of calculations of the IOC (RMOC) using this method in 10 healthy subjects aged 18-23 years, compared with the IOC value determined using the non-invasive monitor system "MARG 10-01" (Microlux, Chelyabinsk), the basis of the work which is the method of tetrapolar bioimpedance rheocardiography (error 15%).

Table 2.
Floor	№	R, cm	MT, kg	Heart rate beats/min	SBP mmHg	DBP mmHg	IOC, ml	RMOC, ml	Deviation %
and	1	154	42	72	117	72	5108	5108	0
	2	157	48	75	102	72	4275	4192	2
	3	172	56	57	82	55	4560	4605	1
	4	159	58	85	107	72	6205	6280	1
	5	164	65	71	113	71	6319	6344	1
6	167	70	73	98	66	7008	6833	3
m	7	181	74	67	110	71	5829	5857	0,2
	8	187	87	69	120	74	6831	7461	9
	9	193	89	55	104	61	6820	6734	1
10	180	70	52	113	61	5460	5007	9
Average deviation between the MOC and RMOC values ​​in these examples	2,79%

The deviation of the calculated value of the IOC from its measured value using the method of tetrapolar bioimpedance rheocardiography in 20 healthy subjects aged 18-35 years averaged 5.45%. The correlation coefficient between these values ​​was 0.94.

The deviation of the calculated values ​​of OPSS and IOC using this method from the measured values ​​can be significant only if there is a significant error in determining the proportionality coefficient K. The latter is possible with deviations in the functioning of the regulation mechanisms of OPSS and/or with excessive deviations from the norm of MT (MT>>P (cm) -101). However, errors in determining TPVR and MOC in these patients can be leveled out either by introducing an amendment to the calculation of the proportionality coefficient (K), or by introducing an additional correction factor into the formula for calculating TPVR. These amendments can be either individual, i.e. based on preliminary measurements of the assessed indicators in a particular patient, and group, i.e. based on statistically identified changes in K and OPSS in a certain group of patients (with a certain disease).

The method is implemented as follows.

To measure heart rate, SBP, DBP, weight and height, any certified devices for automatic, semi-automatic, manual measurement of pulse, blood pressure, weight and height can be used. The subject's heart rate, SBP, DBP, body mass (weight) and height are measured at rest.

After this, the proportionality coefficient (K) is calculated, which is necessary to calculate the OPSS and depends on the body weight (BW), height (P) and gender of the person. For women, K=1 with MT=49 kg and P=150 cm;

at MT≤49 kg K=(MT·P)/7350; at MT>49 kg K=7350/(MT·P).

For men, K=1 with MT=59 kg and P=160 cm;

at MT≤59 kg K=(MT·P)/9440; at MT>59 kg K=9440/(MT·P).

After this, the OPSS is determined using the formula:

OPSS=K·DAD·(Tsts-Tpi)/Tpi,

Tstc=60/HR;

Tpi is the expulsion period, calculated by the formula:

Tpi=0.268·Tsc  0.36 ≈Tsc·0.109+0.159.

The IOC is calculated using the equation:

MOK=Avg.Da·133.32·60/OPSS,

where Avg.Da is the average pressure in the aorta, calculated by the formula:

Avg.Yes=(GARDEN+DBP)/2;

133.32 - amount of Pa in 1 mm Hg;

TPVR - total peripheral vascular resistance (Pa ml -1 s).

The implementation of the method is illustrated by the example below.

Woman - 34 years old, height 164 cm, MT=65 kg, pulse (HR) - 71 beats/min, SBP=113 mmHg, DBP=71 mmHg.

K=7350/(164·65)=0.689

Tsts=60/71=0.845

Tpi≈Tsc·0.109+0.159=0.845·0.109+0.159=0.251

OPSS=K·DAD·(Tsc-Tpi)/Tpi=0.689·71·(0.845-0.251)/0.251=115.8≈116 Pa·ml -1 ·s

Average Yes=(SBP+DBP)/2=(113+71)/2=92 mmHg.

IOC=Avg.Da·133.32·60/OPSS=92·133.32·60/116=6344 ml≈6.3 l

The deviation of this calculated IOC value for this subject from the IOC value determined using tetrapolar bioimpedance rheocardiography was less than 1% (see Table 2, subject No. 5).

Thus, the proposed method allows one to quite accurately determine the values ​​of OPSS and MOC.

BIBLIOGRAPHY

1. Autonomic disorders: Clinic, diagnosis, treatment. / Ed. A.M.Veina. - M.: LLC "Medical information Agency", 2003. - 752 p., p. 57.

2. Zislin B.D., Chistyakov A.V. Monitoring of respiration and hemodynamics in critical conditions. - Ekaterinburg: Socrates, 2006. - 336 p., p. 200.

3. Karpman V.L. Phase analysis of cardiac activity. M., 1965. 275 p., p. 111.

4. Murashko L.E., Badoeva F.S., Petrova S.B., Gubareva M.S. Method for integral determination of central hemodynamic parameters. // RF Patent No. 2308878. Published 10/27/2007.

5. Parin V.V., Karpman V.L. Cardiodynamics. // Physiology of blood circulation. Physiology of the heart. In the series: “Guide to Physiology.” L.: “Science”, 1980. p.215-240., p.221.

6. Filimonov V.I. Guide to general and clinical physiology. - M.: Medical Information Agency, 2002. - pp. 414-415, 420-421, 434.

7. Chazov E.I. Diseases of the heart and blood vessels. Guide for doctors. M., 1992, vol. 1, p. 164.

8. Ctarr I // Circulation, 1954. - V.19 - P.664.

1. A method for determining integral indicators of the state of the cardiovascular system, which consists in determining the total peripheral vascular resistance (TPVR) in healthy subjects, including measuring heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), different in that they also measure body weight (MW, kg), height (P, cm) to determine the proportionality coefficient (K), in women with MT≤49 kg according to the formula K=(MW·P)/7350, with MT>49 kg according to the formula K=7350/(MW·P), for men with MT≤59 kg according to the formula K=(MW·P)/9440, for MT>59 kg according to the formula K=9440/(MW·P), the value OPSS is calculated using the formula
OPSS=K·DAD·(Tsts-Tpi)/Tpi,
where Tc is the period of the cardiac cycle, calculated by the formula
Tstc=60/HR;
Tpi - period of expulsion, Tpi=0.268·Tsc 0.36 ≈Tsc·0.109+0.159.

2. A method for determining integral indicators of the state of the cardiovascular system, which consists in determining the minute blood volume (MBV) in healthy subjects, characterized in that the MVC is calculated using the equation: MVC=Avg.Da·133.32·60/OPSS,
where Av.Da is the average pressure in the aorta, calculated by the formula
Avg.Yes=(GARDEN+DBP)/2;
133.32 - amount of Pa in 1 mm Hg;
TPVR - total peripheral vascular resistance (Pa ml -1 s).

Similar patents:

The invention relates to medical equipment and can be used to perform various medical procedures. .

The resistance of blood vessels is increased when the lumen of the vessel is reduced. A decrease in the lumen of the vessel occurs when:

1. contraction of the muscle layer of blood vessels;
2. swelling of vascular endothelial cells;
3. for certain diseases (atherosclerosis, diabetes mellitus, obliterating endarteritis);
4. at age-related changes in vessels.

The lining of a blood vessel consists of several layers.

The inside of the blood vessel is covered with endothelial cells. They come into direct contact with the blood. With an increase in sodium ions in the blood (excessive consumption of table salt with food, impaired excretion of sodium from the blood by the kidneys), sodium penetrates into the endothelial cells that cover the blood vessels from the inside. An increase in sodium concentration in a cell leads to an increase in the amount of water in the cell. Endothelial cells increase in volume (swell, “swell”). This leads to a narrowing of the lumen of the vessel.

The middle layer of the vascular lining is muscular. It consists of smooth muscle cells that are arranged in a spiral that encircles the vessel. Smooth muscle cells are capable of contracting. Their direction is opposite longitudinal axis vessel (direction of blood movement through the vessel). When they contract, the vessel contracts and the internal diameter of the vessel decreases. When they relax, the vessel expands, the internal diameter of the vessel increases.

The more pronounced muscle layer blood vessel, the more pronounced is the vessel’s ability to contract and expand. There is no possibility of contraction and relaxation in elastic-type arteries (aorta, pulmonary trunk, pulmonary and common carotid arteries), in capillaries, in post-capillary and collecting venules, in fibrous-type veins (veins meninges, retina, jugular and internal mammary veins, veins of the upper body, neck and face, superior vena cava, veins of bones, spleen, placenta). This possibility is most pronounced in the arteries muscular type(cerebral arteries, vertebral, brachial, radial, popliteal arteries and others), less so in arteries of the muscular-elastic type (subclavian, mesenteric arteries, celiac trunk, iliac, femoral arteries and others), in the veins of the upper and lower limbs, partially - in arterioles in the form of precapillary sphincters (smooth muscle cells are located in the form of a ring at the junction of arterioles into capillaries), weakly - in the veins of the digestive tract, muscle venules, in arteriole-venular anastomoses (shunts) and others.

Smooth muscle cells contain protein compounds in the form of threads called filaments. Filaments consisting of the protein myosin are called myosin filaments, and those made of actin are called actin filaments. In the cell, myosin filaments are fixed to dense bodies that are located on the cell membrane and in the cytoplasm. Actin filaments are located between them. Actin and myosin filaments interact with each other. The interaction between actin filaments and myosin filaments causes the smooth muscle cell to contract (contract) or relax (dilate). This process is regulated by two intracellular enzymes: myosin light chain kinase (MLC) and MLC phosphatase. When LCM kinase is activated, smooth muscle cells contract, and when LCM phosphatase is activated, relaxation occurs. The activation of both enzymes depends on the amount of calcium ions inside the cell. When the amount of calcium ions in the cell increases, LCM kinase is activated, and when the amount of calcium ions inside the cell decreases, LCM phosphatase is activated.

Inside the cell (in the cytoplasm of the cell), calcium ions combine with the intracellular protein calmodulin. This compound activates MLC kinase and inactivates MLC phosphatase. LCM kinase phosphorylates myosin light chains (promotes the addition of a phosphate group from adenosine triphosphate (ATP) to LCM. After this, myosin acquires an affinity for actin. Transverse actinomyosin molecular bridges are formed. In this case, actin and myosin filaments are displaced relative to each other. This displacement leads to reduction in the length of the smooth muscle cell. This condition is called contraction of the smooth muscle cell.

When the amount of calcium ions decreases inside the smooth muscle cell, LCM phosphatase is activated and LCM kinase is inactivated. LCM phosphatase dephosphorylates (disconnects phosphate groups from LCM). Myosin loses affinity for actin. Actinomyosin cross bridges are destroyed. The smooth muscle cell relaxes (the length of the smooth muscle cell increases).

The amount of calcium ions inside the cell is regulated by calcium channels on the membrane (shell) of the cell and on the membrane of the intracellular reticulum (intracellular calcium depot). Calcium channels can change their polarity. With one polarity, calcium ions enter the cell cytoplasm, and with the opposite polarity, they leave the cell cytoplasm. The polarity of calcium channels depends on the amount of cAMP (cyclic adenosine monophosphate) inside the cell. With an increase in the amount of cAMP inside the cell, calcium ions enter the cell cytoplasm. When cAMP decreases in the cell cytoplasm, calcium ions leave the cell cytoplasm. cAMP is synthesized from ATP (adenosine triphosphate) under the influence of the membrane enzyme adenylate cyclase, which is in an inactive state on the inner surface of the membrane.

When catecholamines (adrenaline, norepinephrine) combine with α1-smooth muscle cells of blood vessels, activation of adenylate cyclase occurs, which is further interconnected - the amount of cAMP inside the cell increases - the polarity of the cell membrane changes - calcium ions enter the cytoplasm of the cell - the number of calcium ions inside the cell increases - the amount of calmodulin bound increases with calcium - MLC kinase is activated, MLC phosphatase is inactivated - phosphorylation of myosin light chains occurs (attachment of phosphate groups from ATP to LCM) - myosin acquires affinity for actin - actinomyosin cross bridges are formed. The smooth muscle cell contracts (the length of the smooth muscle cell decreases) - in total on the scale of the blood vessel - the blood vessel contracts, the lumen of the vessel (the internal diameter of the vessel) narrows - in total on the scale of the vascular system - vascular resistance increases, increases. Thus, an increase in sympathetic tone (ANS) leads to vasospasm, an increase in vascular resistance and the associated.

Excessive entry of calcium ions into the cell cytoplasm is prevented by the enzyme calcium-dependent phosphodiesterase. This enzyme is activated by a certain (excess) amount of calcium ions in the cell. Activated calcium-dependent phosphodiesterase hydrolyzes (breaks down) cAMP, which leads to a decrease in the amount of cAMP in the cell cytoplasm and interconnectedly changes the polarity of calcium channels in the opposite direction - the flow of calcium ions into the cell decreases or stops.

The functioning of calcium channels is regulated by many substances, both internal and external, that influence calcium channels through connection with certain proteins (receptors) on the surface of smooth muscle cells. Thus, when the parasympathetic ANS mediator acetylcholine combines with the cholinergic receptor of the smooth muscle cell, adenylate cyclase is deactivated, which interconnectedly leads to a decrease in the amount of cAMP and, ultimately, to relaxation of the smooth muscle cell - in total on the scale of the blood vessel - the blood vessel expands, the lumen of the vessel (the internal diameter of the vessel ) increases – in total on the scale of the vascular system – vascular resistance decreases. Thus, an increase in the tone of the parasympathetic ANS leads to vasodilation, a decrease in vascular resistance, and reduces the influence of the sympathetic ANS on the blood vessels.

Note: Axons (processes) of ganglion neurons ( nerve cells) ANS have numerous branches in the thickness of vascular smooth muscle cells. On these branches there are numerous thickenings that perform the function of synapses - areas through which the neuron releases a transmitter when excited.

When protein (AG2) combines with the smooth muscle cell of the vessel, its contraction occurs. If the level of AT2 in the blood is increased for a long time (arterial hypertension), the blood vessels are in a spasmodic state for a long time. High level AT2 in the blood maintains the smooth muscle cells of blood vessels in a state of contraction (compression) for a long time. As a result, hypertrophy (thickening) of smooth muscle cells and excessive formation of collagen fibers develop, the walls of blood vessels thicken, and the internal diameter of blood vessels decreases. Thus, hypertrophy of the muscle layer of blood vessels, which developed under the influence of an excess amount of AT2 in the blood, becomes another supporting factor increased resistance blood vessels, and, therefore, increased blood pressure.

Chapter 4.
Calculated indicators of vascular tone and tissue blood flow in the systemic circulation

Determination of the tone of arterial vessels in the systemic circulation is a necessary element in the analysis of the mechanisms of changes in systemic hemodynamics. It should be remembered that the tone of various arterial vessels has different effects on the characteristics of systemic circulation. Thus, the tone of arterioles and precapillaries offers the greatest resistance to blood flow, which is why these vessels are called resistive, or resistance vessels. The tone of large arterial vessels has less influence on peripheral resistance to blood flow.

The level of mean arterial pressure, with certain reservations, can be thought of as the product of cardiac output and the total resistance of resistive vessels. In some cases, for example, with arterial hypertension or hypotension, it is essential to identify the question of what determines the shift in the level of systemic blood pressure - from changes in cardiac performance or vascular tone in general. In order to analyze the contribution of vascular tone to the noted changes in blood pressure, it is customary to calculate the total peripheral vascular resistance.

4.1. Total peripheral vascular resistance

This value shows the total resistance of the precapillary bed and depends on both vascular tone and blood viscosity. The total peripheral vascular resistance (TPVR) is influenced by the nature of the branching of vessels and their length, so usually the greater the body weight, the lower the TPR. Due to the fact that in order to express OPSS in absolute units, a conversion of pressure into dyn/cm2 (SI system) is required, the formula for calculating OPSS is as follows:

Units of measurement OPSS - dyn cm -5

Methods for assessing the tone of large arterial trunks include determining the speed of propagation of the pulse wave. In this case, it turns out to be possible to characterize the elastic-viscous properties of the vascular wall of both predominantly muscular and elastic types.

4.2. Velocity of pulse wave propagation and modulus of elasticity of the vascular wall

The speed of pulse wave propagation through vessels of elastic (S e) and muscular (S m) types is calculated based on either synchronous recording of sphygmograms (SFG) of the carotid and femoral, carotid and radial arteries, or synchronous recording of ECG and SFG of the corresponding vessels. It is possible to determine C e and C m with synchronous registration of rheograms of the limbs and ECG. Speed ​​calculation is very simple:

S e = L e /T e; S m = L m / T m

where T e is the delay time of the pulse wave in elastic arteries (determined, for example, by the delay in the rise of SFG femoral artery regarding the rise of SFG carotid artery or from the R or S wave of the ECG to the rise of the femoral SFG); Tm is the delay time of the pulse wave in the vessels of the muscular type (determined, for example, by the delay of the SFG of the radial artery relative to the SFG of the carotid artery or the K wave of the ECG); L e - distance from the jugular fossa to the navel + distance from the navel to the pulse receiver on the femoral artery (when using the technique of two SFGs, the distance from the jugular fossa to the sensor on the carotid artery should be subtracted from this distance); L m - the distance from the sensor on the radial artery to the jugular fossa (as when measuring L e, the length to the carotid artery pulse sensor must be subtracted from this value if the technique of two SFGs is used).

The modulus of elasticity of elastic type vessels (E e) is calculated by the formula:

where E 0 - total elastic resistance, w - OPSS. E 0 is found using the Wetzler formula:

where Q is the cross-sectional area of ​​the aorta; T - time of the main oscillation of the pulse of the femoral artery (see Fig. 2); C e - the speed of propagation of the pulse wave through elastic vessels. E 0 can be calculated also by Brezmer and Banke:

where PI is the duration of the expulsion period. N.N. Savitsky, taking E 0 as the total elastic resistance of the vascular system or its volumetric elasticity modulus, proposes the following equality:

where PP is pulse pressure; D - duration of diastole; MAP - mean arterial pressure. The expression E 0 /w can, with a certain error, also be called the total elastic resistance of the aortic wall, and in this case the formula is more suitable:

where T is the duration of the cardiac cycle, MD is mechanical diastole.

4.3. Regional blood flow indicator

In clinical and experimental practice, there is often a need to study peripheral blood flow for the diagnosis or differential diagnosis of vascular diseases. Currently, a fairly large number of methods for studying peripheral blood flow have been developed. At the same time, a number of methods characterize only qualitative features of the state of peripheral vascular tone and blood flow in them (sphygmo- and phlebography), others require complex special equipment (electromagnetic and ultrasonic transducers, radioactive isotopes, etc.) or are feasible only in experimental studies (resistography ).

In this regard, indirect, fairly informative and easily implemented methods that allow quantitative study of peripheral arterial and venous blood flow are of significant interest. The latter include plethysmographic methods (V.V. Orlov, 1961).

When analyzing the occlusion plethysmogram, it is possible to calculate the volumetric blood flow velocity (VVV) in cm 3 /100 tissue/min:

where ΔV is the increase in blood flow volume (cm 3) over time T.

With a slow dosed increase in pressure in the occlusive cuff (from 10 to 40 mm Hg), it is possible to determine venous tone (VT) in mm Hg/cm 3 per 100 cm 3 of tissue using the formula:

where SBP is mean arterial pressure.

To judge functionality vascular wall(mainly arterioles), a calculation of the spasm index (PS) eliminated by a certain (for example, 5-minute ischemia) vasodilatory effect was proposed (N.M. Mukharlyamov et al., 1981):

Further development of the method led to the use of venous occlusive tetrapolar electroplethysmography, which made it possible to detail the calculated indicators taking into account the values arterial inflow and venous outflow (D.G. Maksimov et al.; L.N. Sazonova et al.). According to the developed complex methodology, a number of formulas are proposed for calculating regional blood circulation indicators:

When calculating the indicators of arterial inflow and venous outflow, the values ​​of K 1 and K 2 are found by preliminary comparison of data from the impedance-metric method with data from direct or indirect quantitative research methods, previously tested and metrologically substantiated.

The study of peripheral blood flow in the systemic circulation is also possible using rheography. The principles for calculating rheogram indicators are described in detail below.

Source: Brin V.B., Zonis B.Ya. Physiology of systemic circulation. Formulas and calculations. Rostov University Publishing House, 1984. 88 p.

Literature [show]

1. Alexandrov A.L., Gusarov G.V., Egurnov N.I., Semenov A.A. Some indirect methods for measuring cardiac output and diagnosing pulmonary hypertension. - In the book: Problems of pulmonology. L., 1980, issue. 8, p.189.
2. Amosov N.M., Lshtsuk V.A., Patskina S.A. and others. Self-regulation of the heart. Kyiv, 1969.
3. Andreev L.B., Andreeva N.B. Kinetocardiography. Rostov n/d: Publishing house Rost, u-ta, 1971.
4. Brin V.B. Phase structure of left ventricular systole during deafferentation of sinocarotid reflexogenic zones in adult dogs and puppies. - Pat. physiol, and exp. therapy, 1975, No. 5, p. 79.
5. Brin V.B. Age-related features of the reactivity of the sinocarotid pressor mechanism. - In the book: Physiology and biochemistry of ontogenesis. L., 1977, p.56.
6. Brin V.B. The effect of obzidan on systemic hemodynamics in dogs during ontogenesis. - Pharmacol. and Toksikol., 1977, No. 5, p. 551.
7. Brin V.B. Effect of the alpha-adrenergic blocker pyrroxan on systemic hemodynamics in renovascular hypertension in puppies and dogs. - Bull. exp. biol. and Med., 1978, No. 6, p. 664.
8. Brin V.B. Comparative ontogenetic analysis of the pathogenesis of arterial hypertension. Author's abstract. for the job application uch. Art. doc. honey. Sciences, Rostov n/D, 1979.
9. Brin V.B., Zonis B.Ya. Phase structure of the cardiac cycle in dogs during postnatal otogenesis. - Bull. exp. biol. and med., 1974, No. 2, p. 15.
10. Brin V.B., Zonis B.Ya. Functional state of the heart and pulmonary hemodynamics in respiratory failure. - In the book: Respiratory failure in the clinic and experiment. Abstract. report All conf. Kuibyshev, 1977, p. 10.
11. Brin V.B., Saakov B.A., Kravchenko A.N. Changes in systemic hemodynamics in experimental renovascular hypertension in dogs of different ages. Cor et Vasa, Ed. Ross, 1977, vol. 19, no. 6, p. 411.
12. Vein A.M., Solovyova A.D., Kolosova O.A. Vegetative-vascular dystonia. M., 1981.
13. Guyton A. Physiology of blood circulation. Minute volume of the heart and its regulation. M., 1969.
14. Gurevich M.I., Bershtein S.A. Fundamentals of hemodynamics. - Kyiv, 1979.
15. Gurevich M.I., Bershtein S.A., Golov D.A. and others. Determination of cardiac output by thermodilution method. - Physiol. magazine USSR, 1967, vol. 53, no. 3, p. 350.
16. Gurevich M.I., Brusilovsky B.M., Tsirulnikov V.A., Dukin E.A. Quantitative assessment of cardiac output using the rheographic method. - Medical Affairs, 1976, No. 7, p. 82.
17. Gurevich M.I., Fesenko L.D., Filippov M.M. On the reliability of determining cardiac output using tetrapolar thoracic impedance rheography. - Physiol. magazine USSR, 1978, vol. 24, no. 18, p. 840.
18. Dastan H.P. Methods for studying hemodynamics in patients with hypertension. - In the book: Arterial hypertension. Materials of the Soviet-American symposium. M., 1980, p.94.
19. Dembo A.G., Levina L.I., Surov E.N. The importance of determining pressure in the pulmonary circulation in athletes. - Theory and practice physical culture, 1971, No. 9, p.26.
20. Dushanin S.A., Morev A.G., Boychuk G.K. About pulmonary hypertension in liver cirrhosis and its definition graphic methods. - Medical practice, 1972, No. 1, p. 81.
21. Elizarova N.A., Bitar S., Alieva G.E., Tsvetkov A.A. Study of regional blood circulation using impedancemetry. - Therapeutic archive, 1981, vol. 53, no. 12, p. 16.
22. Zaslavskaya R.M. Pharmacological effects on pulmonary circulation. M., 1974.
23. Zernov N.G., Kuberger M.B., Popov A.A. Pulmonary hypertension V childhood. M., 1977.
24. Zonis B.Ya. Phase structure of the cardiac cycle according to kinetocardiography data in dogs in postnatal ontogenesis. - Magazine evolutionary Biochemistry and Physiol., 1974, v. 10, no. 4, p. 357.
25. Zonis B.Ya. Electromechanical activity of the heart in dogs of various ages normally and with the development of renovascular hypertension, Abstract. dis. for the job application account Candidate of Medical Sciences, Makhachkala, 1975.
26. Zonis B.Ya., Brin V.B. The effect of a single dose of the alpha-adrenergic blocker pyrroxan on cardio- and hemodynamics in healthy people and patients arterial hypertension, - Cardiology, 1979, v. 19, no. 10, p. 102.
27. Zonis Y.M., Zonis B.Ya. On the possibility of determining pressure in the pulmonary circulation using a kinetocardiogram in chronic lung diseases. - Therapist. archive, 4977, vol. 49, no. 6, p. 57.
28. Izakov V.Ya., Itkin G.P., Markhasin B.S. and others. Biomechanics of the heart muscle. M., 1981.
29. Karpman V.L. Phase analysis of cardiac activity. M., 1965
30. Kedrov A.A. An attempt to quantify central and peripheral blood circulation electrometrically. - Clinical Medicine, 1948, v. 26, no. 5, p. 32.
31. Kedrov A.A. Electroplethysmography as a method for objective assessment of blood circulation. Author's abstract. dis. for the job application uch. Art. Ph.D. honey. Sciences, L., 1949.
32. Clinical rheography. Ed. prof. V.T. Shershneva, Kyiv, 4977.
33. Korotkov N.S. On the question of research methods blood pressure. - News of the Military Medical Academy, 1905, No. 9, p. 365.
34. Lazaris Ya.A., Serebrovskaya I.A. Pulmonary circulation. M., 1963.
35. Leriche R. Memories of my past life. M., 1966.
36. Mazhbich B.I., Ioffe L.D., Substitutions M.E. Clinical and physiological aspects of regional electroplethysmography of the lungs. Novosibirsk, 1974.
37. Marshall R.D., Shefferd J. Cardiac function in healthy and healthy patients. M., 1972.
38. Meerson F.Z. Adaptation of the heart to heavy load and heart failure. M., 1975.
39. Methods for studying blood circulation. Under the general editorship of prof. B.I. Tkachenko. L., 1976.
40. Moibenko A.A., Povzhitkov M.M., Butenko G.M. Cytotoxic damage to the heart and cardiogenic shock. Kyiv, 1977.
41. Mukharlyamov N.M. Pulmonary heart. M., 1973.
42. Mukharlyamov N.M., Sazonova L.N., Pushkar Yu.T. Study of peripheral circulation using automated occlusion plethysmography, - Therapist. archive, 1981, vol. 53, no. 12, p. 3.
43. Oransky I.E. Acceleration kinetocardiography. M., 1973.
44. Orlov V.V. Plethysmography. M.-L., 1961.
45. Oskolkova M.K., Krasina G.A. Rheography in pediatrics. M., 1980.
46. Parin V.V., Meerson F.Z. Essays on the clinical physiology of blood circulation. M., 1960.
47. Parin V.V. Pathological physiology of the pulmonary circulation In the book: Guide to pathological physiology. M., 1966, vol. 3, p. 265.
48. Petrosyan Yu.S. Cardiac catheterization for rheumatic diseases. M., 1969.
49. Povzhitkov M.M. Reflex regulation of hemodynamics. Kyiv, 1175.
50. Pushkar Yu.T., Bolshov V.M., Elizarov N.A. and others. Determination of cardiac output by the method of tetrapolar thoracic rheography and its metrological capabilities. - Cardiology, 1977, v. 17, no. 17, p. 85.
51. Radionov Yu.A. On the study of hemodynamics using the dye dilution method. - Cardiology, 1966, vol. 6, no. 6, p. 85.
52. Savitsky N.N. Biophysical basis of blood circulation and clinical methods studying hemodynamics. L., 1974.
53. Sazonova L.N., Bolnov V.M., Maksimov D.G. and others. Modern methods of studying the condition of resistive and capacitive vessels in the clinic. -Therapist. archive, 1979, vol. 51, no. 5, p. 46.
54. Sakharov M.P., Orlova T.R., Vasilyeva A.V., Trubetskoy A.Z. Two components of contractility of the ventricles of the heart and their determination based on non-invasive techniques. - Cardiology, 1980, vol. 10, no. 9, p. 91.
55. Seleznev S.A., Vashtina S.M., Mazurkevich G.S. Comprehensive assessment of blood circulation in experimental pathology. L., 1976.
56. Syvorotkin M.N. On the assessment of myocardial contractile function. - Cardiology, 1963, volume 3, no. 5, p. 40.
57. Tishchenko M.I. Biophysical and metrological foundations of integral methods for determining the stroke volume of human blood. Author's abstract. dis. for the job application uch. Art. doc. honey. Sciences, M., 1971.
58. Tishchenko M.I., Seplen M.A., Sudakova Z.V. Respiratory changes in left ventricular stroke volume healthy person. - Physiol. magazine USSR, 1973, vol. 59, no. 3, p. 459.
59. Tumanovekiy M.N., Safonov K.D. Functional diagnosis of heart diseases. M., 1964.
60. Wigers K. Dynamics of blood circulation. M., 1957.
61. Feldman S.B. Assessment of myocardial contractile function based on the duration of systole phases. M., 1965.
62. Physiology of blood circulation. Physiology of the heart. (Manual of Physiology), L., 1980.
63. Folkov B., Neil E. Blood circulation. M., 1976.
64. Shershevsky B.M. Blood circulation in the pulmonary circle. M., 1970.
65. Shestakov N.M. 0 complexity and disadvantages modern methods determining the volume of circulating blood and the possibility of a simpler and faster method for determining it. - Therapist. archive, 1977, No. 3, p. 115. I. Uster L.A., Bordyuzhenko I.I. On the role of the components of the formula for determining the stroke volume of blood using the method of integral body rheography. -Therapist. zrkhiv, 1978, v. 50, no. 4, p. 87.
66. Agress S.M., Wegnes S., Frement V.P. et al. Measurement of strolce volume by the vbecy. Aerospace Med., 1967, Dec, p.1248
67. Blumberger K. Die Untersuchung der Dinamik des Herzens bein Menshen. Ergebn.Med., 1942, Bd.62, S.424.
68. Bromser P., Hanke S. Die physikalische Bestimiung des Schlagvolumes der Herzens. - Z.Kreislauforsch., 1933, Bd.25, No. I, S.II.
69. Burstin L. -Determination of pressure in the pulmonary by external graphic recordings. -Brit.Heart J., 1967, v.26, p.396.
70. Eddleman E.E., Wilis K., Reeves T.J., Harrison T.K. The kinetocardiogram. I. Method of recording precardial movements. -Circulation, 1953, v.8, p.269
71. Fegler G. Measurement of cardiac output in anesthetized animals by a thermodilution method. -Quart.J.Exp.Physiol., 1954, v.39, P.153
72. Fick A. Über die ilessung des Blutquantums in den Herzventrikeln. Sitzungsbericht der Würzburg: Physiologisch-medizinischer Gesellschaft, 1970, S.36
73. Frank M.J., Levinson G.E. An index of the contractile state of the myocardium in man. -J.Clin.Invest., 1968, v.47, p.1615
74. Hamilton W.F. The physiology of the cardiac output. -Circulation, 1953, v.8, p.527
75. Hamilton W.F., Riley R.L. Comparison of the Fick and dye-dilution method of measuring the cardiac output in man. -Amer.J. Physiol., 1948, v.153, p.309
76. Kubicek W.G., Patterson R.P., Witsoe D.A. Impedance cardiography as a noninvasive method of monitoring cardiac function and other parameters of the cardiovascular system. -Ann.N.Y.Acad. Sci., 1970, v.170, p.724.
77. Landry A.B., Goodyex A.V.N. Hate of rise left ventricular pressure. Indirect measurement and physiological significance. -Acer. J.Cardiol., 1965, v.15, p.660.
78. Levine H.J., McIntyre K.M., Lipana J.G., Qing O.H.L. Force-velocity relations in failing and nonfailing hearts of subjects with aortic stenosis. -Amer.J.Med.Sci., 1970, v.259, P.79
79. Mason D.T. Usefulness and limitation of the rate of rise of intraventricular pressure (dp/dt) in the evaluation of iqyocardial contractility in man. -Amer.J.Cardiol., 1969, v.23, P.516
80. Mason D.T., Spann J.F., Zelis R. Quantification of the contractile state of the intact human heat. -Amer.J.Cardiol., 1970, v.26, p. 248
81. Riva-Rocci S. Un nuovo sfigmomanometro. -Gas.Med.di Turino, 1896, v.50, no. 51, s.981.
82. Ross J., Sobel V.E. Regulation of cardiac contraction. -Amer. Rev. Physiol., 1972, v.34, p.47
83. Sakai A., Iwasaka T., Tauda N. et al. Evaluation of the determination by impedance cardiography. -Soi et Techn.Biomed., 1976, NI, p.104
84. Sarnoff S.J., Mitchell J.H. The regulation of the performance of the heart. -Amer.J.Med., 1961, v.30, p.747
85. Siegel J.H., Sonnenblick E.N. Isometric Time-tension relationship as an index of ocardial contractility. -Girculat.Res., 1963, v.12, p.597
86. Starr J. Studies made by simulating systole at necropsy. -Circulation, 1954, v.9, p.648
87. Veragut P., Krayenbuhl H.P. Estimation and quantification of myocardial contractility in the closed-chest dog. -Cardiologia (Basel), 1965, v.47, no. 2, p.96
88. Wezler K., Böger A. Der Feststellung und Beurteilung der Flastizitat zentraler und peripherer Arterien am Lebenden. -Schmied.Arch., 1936, Bd.180, S.381.
89. Wezler K., Böger A. Über einen Weg zur Bestimmung des absoluten Schlagvolumens der Herzens beim Menschen auf Grund der Windkesseltheorie und seine experimentalle Prafung. -N.Schmied. Arch., 1937, Bd.184, S.482.