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PubMed1976

Hemodynamic effect of pindolol in essential hypertension with special reference to the resistance and capacitance vessels of the forearm.

Ten patients, mean age 48 years, with essential hypertension of stage I and II according to the WHO classification, have been studied at rest and during work before and after on average 8 weeks oral treatment with a beta-adrenergic blocking agent, pindolol. The pindolol treatment caused a significant decrease in the systemic systolic and diastolic blood pressure, heart rate and cardiac output both at rest and during work. The systemic vascular resistance and the forearm vascular resistance decreased significantly after and during work, respectively. Forearm venous tone was significantly decreased at rest, during and after work. The plasma renin activity decreased. Three mechanisms seem to be involved in the antihypertensive effect of pindolol: 1) a negative chronotropic effect on the heart, 2) a decrease in peripheral vascular resistance, and 3) an increase in vascular capacitance affecting the venous return.

Adult↗
PubMed1984

Theoretical advantages of abdominal counterpulsation in CPR as demonstrated in a simple electrical model of the circulation.

Recent animal studies and preliminary clinical observations suggest that the addition of interposed abdominal compressions (IAC) to ventilation and chest compression of standard cardiopulmonary resuscitation (CPR) augments blood flow, blood pressures, and immediate survival. To investigate the physical basis for enhanced circulation during IAC-CPR, we developed an electrical model of the circulation. Heart and blood vessels were modeled as resistive-capacitive networks, pressures as voltages, blood flow as electric current, blood inertia as inductance, and the cardiac and venous valves as diodes. External pressurization of the heart and great vessels, as would occur in CPR, was simulated by application by half-sinusoidal voltage pulses between vascular capacitances and ground. Closed-chest CPR was simulated by pressurization of all intrathoracic capacitances. IAC was simulated by similar pressurization of the inferior vena cava and abdominal aorta, 180 degrees out of phase with chest compression. During simulation of CPR, IAC improved cranial and myocardial perfusion at all levels of chest compression pressure by amounts linearly related to peak abdominal pressure, suggesting that the abdomen can function as a second, independent blood pump during CPR. Brain and heart flow were improved further during simulated vasoconstriction in kidneys, abdominal viscera, and extremities. Based on the fundamental properties of the cardiovascular system represented in the model, abdominal counterpulsation provides a rational basis for flow augmentation during CPR.

Blood Circulation↗
PubMed1975

Vascular volume-distensibility characteristics of the isolated dogfish gut.

The vascular capacitance and volume distensibility of the isolated dogfish gut and segments of dogfish arteries and veins were investigated. The volume-distensibility curves for dogfish arteries and veins are very similar to comparable curves derived from arteries and veins of dogs or man. The vascular volume-distensibility curve of the gut, however, shows a greater distensibility at higher systemic pressure than at lower pressure. Evidence is presented that significant amounts of fluid leave the vascular compartment at a lower systemic pressure than in an isolated dog hindlimb preparation. However, this alone does not explain the atypical vascular volume-distensibility curve obtained from the dogfish gut. It is suggested that in the dogfish capillary filtration pore enlargement takes place at a very low capillary pressure or volume (compared to mammals) and this complicates the construction of a volume-distensibility curve because initial vascular volume is not constant.

Animals↗
PubMed1992

Haemodynamic studies during the management of severe tetanus.

Detailed invasive haemodynamic studies were performed in 27 of 32 patients with severe tetanus. Nineteen had severe uncomplicated tetanus and eight had associated major complications, chiefly infection and pulmonary complications. The results were compared with those obtained from 15 healthy male volunteers who served as controls. There were two deaths in 32 patients (mortality 6.25 per cent). Severe tetanus without major complications was characterized by a high output hyperkinetic circulatory state with tachycardia (heart rate 131 (19.2) beats/minute), increased stroke volume index (43.1 (10.7) ml/m2), increased cardiac index (5.48 (0.94) l/min/m2) and a normal left ventricular stroke work index (60.5 (15.9) g/m/m2). Volume loading demonstrated a significant haemodynamic response and increased vascular capacitance. Even so the maximum percent rise from baseline values of these indices after volume load was significantly higher in controls (p < 0.001). Autonomic cardiovascular disturbances affected both sympathetic and parasympathetic activity. Hypertension and tachycardia alternating with hypotension and bradycardia were related to sudden fluctuations in systemic vascular resistance. Our studies suggested some degree of myocardial dysfunction in patients with severe uncomplicated tetanus. The haemodynamics of severe tetanus were masked and altered by complicating infection, pneumonia, and atelectasis.

Acute Disease↗
PubMed1990

Model-based analysis of transmural vessel impedance and myocardial circulation dynamics.

The basic structure of a model of the coronary circulation has been developed to explain the relationship between transmural perfusion dynamics and intramyocardial mechanics. The model is in the form of a topologically isomorphic network representation and incorporates experimentally measured time-varying perfusion and intramyocardial pressure sources as driving inputs to the model. The intramyocardial vessels are treated as nonlinear impedance elements possessing regional external pressure-dependent resistance and capacitance. Three circuit branches, perfusing the epicardial, subepicardial, and subendocardial muscle layers, are mathematically modeled and are used to predict time-dependent flow within the left ventricular myocardium. The phasic coronary blood flow characteristics predicted by the model exhibit waveform patterns that correlate qualitatively with those patterns measured experimentally. In addition, the pressure-dependent vascular capacitance induces a sustained (out of phase with arterial inflow) venous systolic flow. The model also exhibits retrograde systolic subendocardial flow and stop-flow pressure, which are dependent on coronary resistive and capacitive properties and on the perfusion pressure decay time constant. Furthermore, the results predict an abrupt decrease in subendocardial flow with perturbation of either arteriolar or capillary bed compliance. The model describes time-dependent intramyocardial properties that have been confusing and controversial in the understanding of coronary circulation dynamics. Several steps are identified that are expected to improve and refine the model significantly.

Animals↗
PubMed1979

[Adrenergic mechanisms of changes in the resistance and volume vessels of the small intestine in the presence of a reduced volume of circulating blood].

In humorally isolated small intestine, the 10--20%--decrease in the perfusing blood volume against the background of augmented vascular resistance of the small intestine, induces different shifts of the latter's vascular capacitance. At the blockade of small intestine's beta--adrenoreceptors the decrease does not practically tell on the character of shifts in the intestine's resistance and capacitance while the blockade of alpha--adrenoreceptors abolishes the augmentation of these parameters.

Animals↗
PubMed1999

Numerical simulation of the hemodynamic response to hemodialysis-induced hypovolemia.

To provide a framework for analyzing cardiovascular response to hemodialysis-induced hypovolemia, we developed a computer model which simulates arterial pressure changes caused by loss of blood volume. The model includes arterial and venous systemic circulation, Starling's law and inotropic regulation of heart, arterial and cardiopulmonary baroreflex control of capacitance, and resistance vessels. The performance of this model was assessed by analyzing the hemodynamic responses recorded in 12 patients undergoing chronic hemodialysis, 6 classified as hypotension resistant (stable group) and 6 as hypotension prone (unstable group). Arterial pressure, heart rate, and blood volume were recorded during regular hemodialysis. Blood volume and heart rate were used as inputs to the simulator whereas the arterial pressure response obtained by simulation was fitted to the measured data by tuning simulator parameters relative to the capacitance and resistance controls. Although analyzed pressure responses exhibited a wide variety of time patterns, for each one it was possible to identify an optimal set of parameters allowing the recorded pressure data to be accurately reproduced by the model. Sensitivity analysis performed with the model indicated that pressure response strongly depends on the parameter Kv accounting for the capability to control vascular capacitance. According to these results, the parameter Kv in the stable group was 9 times that of the unstable group, thereby suggesting a possible cause of their different hemodynamic behavior.

Analysis of Variance↗
PubMed1983

In vivo and in vitro studies to elucidate the hemodynamic differences of sodium nitroprusside, nitroglycerin, and two isosorbide nitrates.

In isolated renal veins of the rabbit, isosorbide dinitrate and isosorbide-5-mononitrate were seven to twenty times more potent as relaxants than in renal arteries which explains their predilection for the capacitance vascular bed in vivo. For sodium nitroprusside (SNP) and nitroglycerin (NTG), the sensitivity was slightly greater in veins at threshold concentrations (EC10), but similar in veins and arteries at higher concentrations (EC50). After 30 min of exposure, the relaxant effect to NTG faded partially in arteries, but not in veins, which may underlie its preference for the capacitance vessels in vivo. In anaesthetized rats, SNP and NTG were infused i.v. or into the femoral artery. The hypotensive response to NTG was the same by either route of infusion, whereas that to SNP was considerably lower on infusion into the femoral artery; a 34% inactivation of SNP on passage through the hind leg was calculated. The result decrease in venous over arterial blood levels of SNP at a somewhat greater sensitivity of veins than of arteries may account for the balanced effect of SNP on resistance and capacitance vessels in vivo.

Animals↗
PubMed1991

Blood volume changes in liver and spleen during cardiogenic shock in dogs.

Changes in vascular capacitance of the liver and spleen were studied in seven anesthetized dogs during cardiogenic shock induced by coronary microembolization. Left ventricular end-diastolic pressure increased from 2 +/- 2 to 28 +/- 4 mmHg (P less than 0.001), and mean aortic pressure decreased from 111 +/- 7 to 56 +/- 9 mmHg (P less than 0.001). Hepatic venous pressure increased from 1.8 +/- 0.6 to 5.0 +/- 1.0 mmHg (P less than 0.05). Portal venous pressure did not change. Blood volume changes were assessed from sonomicrometric measurements of organ diameters. Hepatic diameter increased after embolization, corresponding to an estimated 54 +/- 14 ml increase of hepatic blood volume (P less than 0.01). Splenic diameter gradually decreased during shock until an estimated 33 +/- 12 ml of blood had been released (P less than 0.05). Occlusion of hepatic venous outflow by a balloon catheter was used to cause ramp changes in hepatic volume and hepatic venous pressure so that a pressure-volume curve could be estimated. Analysis of the hepatic curves showed an increase in unstressed volume with no change in vascular compliance during shock. The blood volume increase could in part be attributed to increased outflow pressure, but active dilation of hepatic capacitance vessels probably contributed. Splenic curves were shifted downward, suggesting expulsion of blood by active contraction.

Animals↗
PubMed1999

Effects of inhaled nitric oxide on pulmonary hemodynamics in a porcine model of endotoxin shock.

OBJECTIVE: To evaluate the effects of inhaled nitric oxide (NO) on pulmonary circulation in a porcine endotoxin shock model. DESIGN: Prospective, randomized trial. SETTING: Laboratory at a large university medical center. SUBJECTS: Twelve pathogen-free pigs weighing 15 to 31 kg. INTERVENTIONS: After surgical preparation, all pigs received a 0.5 mg/kg endotoxin infusion over 30 mins. One hour after the start of endotoxin, NO inhalation (40 ppm) was initiated in six pigs, whereas the six remaining pigs served to control the progression of shock in this model. Consecutive changes in systemic and pulmonary hemodynamics, including characteristic resistance, vascular compliance, peripheral vascular resistance, and inductance, were continuously assessed during the experimental protocol using a four-element Windkessel model of the pulmonary circulation. MEASUREMENTS AND MAIN RESULTS: Endotoxin insult resulted in a biphasic pulmonary artery pressure increase from 14 +/- 2 to 32 +/- 4 mm Hg. Inhaled NO reversed the resistance to blood flow in small pulmonary arteries from 596 +/- 69 to 424 +/- 36 dyne-sec/ cm5. In contrast, the vascular capacitance of the entire pulmonary circuit, which decreased from 2.4 +/- 0.2 to 0.8 +/- 0.1 mL/mm Hg throughout endotoxin challenge, remained insensitive to NO administration. CONCLUSION: In endotoxin-induced pulmonary hypertension, inhaled NO may function as a modulator of distal pulmonary arterial tone but fails to act as a regulator of larger capacitance pulmonary vessels.

Administration, Inhalation↗
PubMed1984

Control of hemodynamic adjustments during acute volume expansion in the rabbit.

The influence of reflexes mediated by the carotid sinus, aortic, and vagus nerves on control of blood pressure were investigated in the pentobarbital-anesthetized rabbit during an acute intravascular volume expansion. Blood, kept at 37 degrees C, was gradually infused at 2.5-min intervals until the blood volume of each animal was expanded to 10, 20, 30, and 40% above normal. Responses in sinoaortic-vagally denervated rabbits were compared to intact rabbits. Both intact and denervated animals showed a significant increase in central venous pressure with each 10% addition of blood. Heart rate did fall significantly in the intact group but not in the denervated group. No significant changes were identified in mean arterial pressure (MAP) in either group. In both groups changes in cardiac output were significantly greater than control for 20, 30, and 40% expansion and calculated total peripheral resistance fell in both groups at all levels of expansion when compared to control. The absence of significant changes in MAP within the intact and denervated groups suggests that sinoaortic-vagal reflexes are not affecting control of MAP in response to slow, acute volume expansion in the intact rabbit. On the other hand, since total peripheral resistance fell in both groups, a non-sinoaortic-vagal mechanism appears to be functional. This mechanism may assist in increasing vascular capacitance in order to prevent significant increases in blood pressure.

Animals↗
PubMed1988

Dynamic changes in venous outflow by baroreflex and left ventricular distension.

We examined the dynamic changes in venous outflow from the splanchnic and extrasplanchnic vascular beds in response to carotid sinus (CS) baroreflex and left ventricular (LV) distension in 12 dogs anesthetized with pentobarbital sodium. Splenic sympathetic nerve activity was measured in an additional group of six dogs. A heart-lung bypass was used with constant cardiac output and constant venous pressure. LV distension was produced by inflating a balloon in the LV. LV distension and an increase in CS pressure from 50 to 200 mmHg decreased blood pressure by 26 +/- 5 and 30 +/- 6 mmHg and increased vascular capacitance by 5.5 +/- 0.9 and 4.5 +/- 1.2 ml/kg, respectively. Splanchnic venous outflow exhibited a transient decrease, whereas extrasplanchnic venous outflow showed a transient increase, in response to LV distension and increasing CS pressure, accompanied by a sustained decrease in splenic nerve activity. The results indicate important differences between splanchnic and extrasplanchnic components of the total venous system in terms of the regulation of venous capacitance. It is suggested that changes in venous capacitance produced by LV distension and CS baroreflex are primarily due to active changes in splanchnic venous tone.

Animals↗
PubMed1983

Comparison of isogravimetric and venous occlusion capillary pressures in isolated dog lungs.

Venous occlusion capillary pressures (Pcv) were simultaneously compared with isogravimetric capillary pressures (PcI) in the same isolated perfused dog lung preparations. For 26 determinations, PcI averaged 1.23 +/- 0.22 (SE) mmHg higher than Pcv. However, the two measurements of capillary pressure were highly correlated (r = 0.99), and the following regression equation was obtained: Pcv = 1.12 PcI - 2.1. Pcv could be easily measured several times in the same preparation, either by total venous occlusion or regional venous occlusion using a Swan-Ganz balloon catheter. In addition, Pcv did not require an isogravimetric state for its determination. These data suggest that the major sites of filtration and vascular capacitance in the pulmonary circulation reside in the microvessels and that the more easily determined Pcv is an adequate measure of the average capillary filtration pressure in the lungs.

Animals↗
PubMed1986

Physiology of venous return. An unappreciated boost to the heart.

Adequate cardiovascular function depends on the control of venous tone as well as cardiac contractility, heart rate, vascular resistances, and an adequate blood volume. Venous tone is a major determinant of cardiac preload, a clinically important factor influencing cardiac function, especially during cardiac failure. In this review, vascular capacitance, venous tone, and venous return are discussed, and the concepts relating them to cardiovascular function are summarized. Active venoconstriction or dilation provides a rapid compensation, equivalent to a change in blood volume, for cardiovascular homeostasis.

Blood Circulation↗
PubMed1998

Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits.

Changes in hepatic venous resistance were estimated in rabbits from the hepatic venular-inferior vena caval pressure gradient [servo-null micropipettes in 49 +/- 15 (SD) microns vessels] and the total hepatic blood flow (ultrasound probe encircling the hepatic artery and the portal vein). Changes in liver volume, and thus vascular capacitance, were estimated from measures of the liver lobe thickness. Norepinephrine (NE), isoproterenol (Iso), adenosine (Ado), histamine (Hist), or acetylcholine (ACh) was infused into the portal vein at a constant rate for 5 min. NE, Hist, and Ado increased hepatic venular pressure, but only NE and Hist significantly increased hepatic venular resistance. NE reduced the liver thickness, but Hist and Ado caused engorgement. Hepatic blood flow was increased by NE and Ado and decreased by ACh. The influence of intraportal vein infusion of Iso on the liver vasculature, at doses similar to that of NE, was insignificant. We conclude that NE acted on all the hepatic microvasculature, increasing resistance and actively decreasing vascular volume. Hist passively induced engorgement by increasing outflow resistance, whereas the liver engorgement seen with Ado was passively related to the increased blood flow. ACh constricted the portal venules but did not change the liver volume.

Acetylcholine↗
PubMedDate not supplied

[Direct assessment of mesenteric vein compliance in the rat during pregnancy].

This study was designed for two purposes. The first was to establish an in-vitro technique for the comparative study of isolated capacitance veins during pregnancy. Secondly, to test the hypothesis that pregnancy is associated with an increase in venous compliance and the unstressed volume of the veins. Capacitance-size mesenteric veins were mounted in a pressurized myograph system equipped with a video dimension analyzing system and a servo pressure control unit, which was modified for venous studies. After equilibration, the transmural pressure was changed from 2 to 10 mmHg in 2 mmHg increments every 15 minutes. The calculated change in volume over this pressure range consisted of both a change in vessel diameter and in axial length. The veins from the nonpregnant rats exhibited a greater change in axial length than those from the pregnant rats (21% vs. 14%). Unexpectedly, the compliance (change in volume/change in pressure) of the veins from the pregnant rats was significantly less (42%) than those from the nonpregnant rats. However, the basic component of the change in vascular capacitance, the unstressed volume, was significantly greater in the veins from the pregnant rats (100%). We conclude that pregnancy causes alterations in the wall of the capacitance veins, which results in an apparent increase in volume at the expense of wall compliance. Secondly, the pressurized myograph system is a valuable tool for studying the physiology of the capacitance veins during pregnancy under rigorously controlled conditions.

Animals↗
PubMed1995

Isoflurane-mediated inhibition of the constriction of mesenteric capacitance veins and related circulatory responses to acute graded hypoxic hypoxia.

We measured the effects of inhaled isoflurane on hypoxemia-induced changes in the diameter of small mesenteric (capacitance-regulating) veins, sympathetic efferent neural activity, heart rate, and arterial blood pressure. Simultaneous changes in these dependent variables were measured in situ in response to 40-s periods of sequentially administered 10%, 5%, 2.5%, and 0% inspired oxygen before, during, and after either 0.75% or 1.5% vol/vol inhaled isoflurane in alpha-chloralose-anesthetized rabbits. Isoflurane inhibited hypoxia-mediated venoconstriction, increases in sympathetic efferent nerve activity, arterial hypertension, and bradycardia. Furthermore, inhibition of diameter, blood pressure, and heart rate responses persisted after washout of isoflurane. Differences in the attenuation of these respective hypoxia-mediated responses were minimal between the two concentrations of inhaled isoflurane. These results further demonstrate that isoflurane alters the ability to produce cardiovascular adjustments to circulatory stress, including changes in vascular capacitance, which is a major regulatory mechanism.

Acute Disease↗
PubMed1988

Use of acetylcholine to measure total vascular pressure-volume relationship in dogs.

To define total vascular capacitance, we used acetylcholine to arrest the heart and measured mean circulatory filling pressure (MCFP) during controlled hemorrhage and volume loading in 12 splenectomized dogs after ganglion blockade with hexamethonium. We also examined the gross pathological and histological changes in the lungs. Controlled hemorrhage (n = 12) of 5 and 10 ml/kg decreased MCFP from 6.8 +/- 0.1 to 4.9 +/- 0.3 and 3.6 +/- 0.2 mmHg, respectively. Volume loading of 5 (n = 8) and 10 ml/kg (n = 4) increased MCFP to 9.3 +/- 0.2 and 12.1 +/- 0.1 mmHg, respectively. At MCFPs below 5 mmHg, the pressure (P)-volume (V) relationship was not linear [(P = P0ekV, where k is slope of ln (MCFP) vs. V, k = 0.061, R2 = 0.998]. At MCFPs between 5 and 12 mmHg, the pressure-volume relationship was linear (slope = 0.479 mmHg.ml-1.kg-1, R2 = 0.992) and total vascular compliance was 2.09 ml.mmHg-1.kg-1. There were no changes in heart rate, cardiac output, right atrial, pulmonary artery, and pulmonary artery wedge pressures when values at base line were compared with those measured 15 min after each arrest. There were no changes in arterial gas measurements or acid-base balance, and there was no evidence of atelectasis or interstitial or intra-alveolar edema. We conclude that the total body pressure-volume relationship in the presence of ganglion blockade had a nonlinear configuration. The use of acetylcholine to arrest the heart, four times with hexamethonium in reflex-blocked animals, did not result in changes in hemodynamics or pulmonary function.

Acetylcholine↗