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At least 19 recordsLinked to original sources
PubMed1980

[Capacitive vascular reactions of the skeletal musculature before and after adrenoreceptor blockade].

In acute experiments on cats under autoperfusion of the denervated shank vessels with a constant blood volume, injection of noradrenaline into the perfusate could either decrease or increase vascular capacitance. The character and magnitude of reaction depended on the initial level of venous pressure: in pressure 10--15 Hg the decrease was predominant, whereas in pressure 0 and 25 mm Hg--the increase of vascular capacitance occurred. Under blockade of beta-adrenoreceptors with propranolol the dependence of the character of changes in shank vessels capacitance remained the same. Under dihydroergotoxin blockade of alpha-adrenoreceptors, noradrenaline produced only an insignificant increase of the vascular capacitance.

Animals↗
PubMed1988

Left ventricular reflex control of venous return and systemic vascular capacitance in dogs.

The reflex effects of left ventricular distension on venous return, vascular capacitance, vascular resistance, and sympathetic efferent nerve activity were examined in dogs anesthetized with sodium pentobarbital. In addition, the interaction of left ventricular distension and the carotid sinus baroreflex was examined. Vascular capacitance was assessed by measuring changes in systemic blood volume, using extracorporeal circulation with constant cardiac output and constant central venous pressure. Left ventricular distension produced by balloon inflation caused a transient biphasic change in venous return; an initial small increase was followed by a late relatively large decrease. Left ventricular distension increased systemic blood volume by 3.8 +/- 0.6 mL/kg and decreased systemic blood pressure by 27 +/- 2 mmHg (1 mmHg = 133.3 Pa) at an isolated carotid sinus pressure of 50 mmHg. These changes were accompanied by a simultaneous decrease in sympathetic efferent nerve activity. When the carotid sinus pressure was increased to 125 and 200 mmHg, these responses were attenuated. It is suggested that left ventricular mechanoreceptors and carotid baroreceptors contribute importantly to the control of venous return and vascular capacitance.

Animals↗
PubMed1986

Vascular capacitance responses to hypercapnia of the vascularly isolated head.

Hypercapnic stimulation of the brain may account for some of the decrease in vascular capacitance (venoconstriction) seen with whole-body hypercapnia. Six mongrel dogs were anesthetized with alpha-chloralose and paralyzed with pancuronium bromide. The vagi were cut and the carotid bodies and sinuses were denervated. The head circulation was isolated and perfused with normoxic [arterial partial pressure of O2 (Pao2) = 112 mmHg], normocapnic (PaCO2 = 40 mmHg) blood, or one of three levels of normoxic, hypercapnic (PaCO2 = 56, 68, or 84 mmHg) blood. A membrane oxygenator was used to change gas tensions in the perfusate blood. The systemic circulation received normoxic, normocapnic blood (Pao2 = 107 mmHg; PaCO2 = 32 mmHg). Systemic arterial pressure increased from 111 to 134 mmHg, and heart rate decreased from 174 to 150 beats/min with a head blood PaCO2 of 84 mmHg. Central blood volume was not affected by head hypercapnia. Cardiac output significantly decreased only with a head blood PaCO2 of 84 mmHg. Mean circulatory filling pressure increased by 0.014 mmHg/1 mmHg increase in head PaCO2. The sensitivity of the total peripheral resistance to cephalic blood hypercapnia was 0.88%/mmHg, whereas that for the mean circulatory filling pressure was only 0.19%/mmHg. We conclude that stimulation of the brain, via perfusion of the head with hypercapnic blood, causes a small but significant increase in mean circulatory filling pressure, due to systemic venoconstriction.

Animals↗
PubMed1997

Beta-adrenoceptors in vascular capacitance responses to unloading of carotid baroreceptors in anesthetized dogs.

The role of beta- and alpha-adrenoceptors in the total vascular capacitance responses to changing pressure in vascularly isolated carotid sinuses of anesthetized and atropinized dogs was investigated. A change in vascular capacitance was determined by measuring the shift of blood in and out of a reservoir that was connected to the aorta and maintained at a constant pressure. Changes in carotid sinus pressure from 135 to 57 mmHg and back to 137 mmHg resulted in a rapid vascular capacitance response of approximately 30 ml in the absence of adrenoceptor antagonists. Administration of a beta2-adrenoceptor antagonist (ICI-118551) caused a significant enhancement of the capacitance responses to similar decreases and increases in carotid sinus pressure (approximately 130%). Administration of a beta1-adrenoceptor antagonist (CGP-20712A) did not cause any further enhancement of the responses. However, an alpha-blocker (phentolamine) reduced the responses by 75%. The results suggest that in the presence of a beta2-adrenoceptor antagonist vascular capacitance responses to loading and unloading of baroreceptors are greatly enhanced and that patients suffering from orthostatic syncope may benefit from this kind of drug.

Adrenergic beta-Antagonists↗
PubMed1993

Captopril attenuates pacing-induced acute heart failure by increasing total vascular capacitance.

To study the effects of captopril pretreatment on vascular capacitance in acute heart failure, anesthetized splenectomized dogs were subjected to rapid right ventricular pacing (RRVP) at 250 beats/min for 60 min combined with an intravenous (i.v.) 20-ml/kg volume load of dextran 70 over 10 min. Captopril pretreatment [50 mg every 8 h for 3 days plus 0.5 mg/kg intravenously (i.v.) at induction of anesthesia] attenuated development of acute heart failure associated with RRVP, maintaining normal cardiac output (CO) and pulmonary capillary wedge pressures (PCWP). Total vascular capacitance after a volume load plus RRVP was higher in captopril-pretreated animals (129.8 +/- 3.2 vs. 100.4 +/- 4.8 ml/kg) owing to an increase in unstressed volume (118.6 +/- 3.1 vs. 88.4 +/- 5.6 ml/kg). Arterial capacity and pulmonary (central) vascular capacitance were also increased.

Acute Disease↗
PubMed1989

Influence of lung inflation reflex on vascular capacitance in the systemic circulation.

The effects of sustained lung inflation on systemic vascular capacitance (SVC), systemic vascular resistance (SVR), and cardiac sympathetic efferent nerve activity (SENA) were investigated in anesthetized dogs. By use of a total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10, 15, and 20 mmHg. Tracheal pressures of 10, 15, and 20 mmHg increased system vascular capacitance by 1.4, 3.1, and 4.3 ml/kg and decreased systemic vascular resistance by 0.11, 0.15, and 0.16 mmHg.kg.min-ml-1, respectively, at low carotid sinus pressure (CSP) of 41 mmHg. SENA showed a concomitant decrease. Bilateral vagotomy attenuated the change in SVR by 69%, SVC by 62%, and SENA by 97% when lungs were inflated to a tracheal pressure of 20 mmHg at a low CSP. These results indicate that lung inflation causes a reflex induced increase in SVC as well as a decrease in both SVR and SENA. The lung inflation reflex is mediated primarily through vagal afferent nerve fibers with a small contribution from other afferent nerve pathways.

Animals↗
PubMed1991

Whole body vascular capacitance response to vasopressin is mediated by autonomic function.

Effects of intravenous infusions of arginine vasopressin (AVP) on whole body vascular capacitance were determined in anesthetized cats when autonomic nervous system function was intact and, in other cats, when reflexes were blocked by the ganglionic blocking agent pentolinium. With the use of the constant cardiac output-reservoir technique, changes in reservoir volume were assumed to reflect reciprocal changes in whole body vascular capacitance. Relationships between the dose of AVP and the plasma concentration of the peptide achieved during infusions were not significantly different in the two groups of animals. Blood pressure responses to AVP were greater, whereas heart rate responses to the peptide were abolished in ganglion-blocked cats. In cats with intact autonomic function, reservoir volume decreased by 1.6, 4.2, and 7.8 ml/kg at AVP doses of 1, 10, and 100 ng.kg-1.min-1, respectively. In contrast, in ganglion-blocked cats, reservoir volume did not change significantly at 1.0 and 10 ng.kg-1.min-1 of AVP, and the highest dose caused a much smaller change in volume (3 ml/kg) than that observed in cats with intact autonomic function (7.8 ml/kg). Systemic compliance was unchanged by AVP in both groups of animals, suggesting that the increases in whole body vascular capacitance were likely due to changes in unstressed volume. The results suggest that reflexively mediated changes in autonomic function increase whole body vascular capacitance during elevations in the circulating levels of AVP to plasma concentrations that are biologically relevant. These findings may explain how AVP decreases cardiac output in animals with an intact autonomic nervous system.

Animals↗
PubMed1993

Vascular capacitance following preoptic recess lesions.

Vascular capacitance was studied in anesthetized control (CONT) animals and in rats after electrolytic ablation of the periventricular tissue surrounding the anteroventral third cerebral ventricle (AV3V-X). Blood volume (BV) was determined by use of radiolabeled serum albumin, and mean arterial pressure (MAP) and central venous pressure (CVP) were continuously measured. Mean circulatory filling pressure (MCFP) was calculated by use of MAP and CVP obtained during circulatory arrest induced by inflation of a right atrial balloon during BV expansion and contraction. MCFP-BV relationships were calculated to estimate vascular compliance. CONT and AV3V-X animals were tested after treatment with both vehicle and hexamethonium, a ganglionic blocking agent. BV, MAP, and CVP were similar between CONT and AV3V-X animals. However, MCFP was significantly lower in AV3V-X animals (4.6 +/- 0.3 mmHg) than in CONT rats (6.6 +/- 0.5 mmHg). Furthermore, AV3V ablation caused a significant shift of the MCFP-BV relationship toward the volume axis with no change in compliance, indicating decreased venous tone. Finally, hexamethonium treatment significantly reduced MCFP in CONT animals (3.8 +/- 0.7 mmHg) and shifted the MCFP-BV line toward the BV axis but had no effect on these measures in AV3V-X animals. These data indicate that electrolytic ablation of AV3V periventricular tissue significantly reduces venous tone by decreasing neurally mediated venoconstriction.

Animals↗
PubMed1991

Effects of nitroglycerin and nitroprusside on vascular capacitance of anesthetized ganglion-blocked dogs.

To determine whether changes in vascular capacitance induced by nitroglycerin (NTG) and nitroprusside were due to changes in compliance or unstressed vascular volume, doses producing similar reductions in arterial pressure (Psa) were studied on separate days in six dogs anesthetized and ventilated with pentobarbital after splenectomy during ganglion blockade with hexamethonium. Mean circulatory filling pressure (Pmcf) was determined during transient circulatory arrest induced by acetylcholine at baseline blood volumes and after increases of 5 and 10 ml/kg. Central blood volumes (CBVs, pulmonary artery to aortic root) were determined from transit times, and separately measured cardiac output (CO) was estimated by thermodilution (right atrium to pulmonary artery). NTG and nitroprusside produced similar reductions in Psa and Pmcf without significantly altering right atrial pressure (Pra), pressure gradient for venous return, or CO. Total vascular compliance was not altered, but total vascular capacitance was increased on an average of 4.0 +/- 1.4 ml/kg after NTG and 3.0 +/- 1.3 ml/kg after nitroprusside by increases in unstressed volume. Both drugs caused a variable reduction in CBV, averaging 2 ml/kg. Thus, both drugs produced a large increase in peripheral venous capacitance by increasing unstressed vascular volume without altering total vascular compliance.

Acetylcholine↗
PubMed1988

Increased pulmonary vascular capacitance with beta-adrenergic receptor stimulation: an experimental study of the effect of isoproterenol on the pulmonary vascular volume-pressure relationship.

The present study is an investigation of the effect of beta-adrenergic receptor stimulation by isoproterenol on pulmonary vascular capacitance. The experiments were done in six intact-chest, anaesthetized dogs in which pulmonary and cardiac blood volumes were assessed by blood pool scintigraphy. Isoproterenol (0.150 microgram.kg-1.min-1) significantly (p less than 0.005) lowered pulmonary capillary wedge pressure (PPCW) and pulmonary artery pressure (PPA) but did not significantly change pulmonary blood volume (PBV). Left ventricular end-diastolic pressure and total cardiac volume both significantly (p less than 0.005) decreased. Pulmonary vascular volume-pressure (V-P) relationships before and during isoproterenol were described by means of blood transfusions and hemorrhage. In individual dogs the PBV-PPCW and the PBV-(PPCW + PPA)/2 relationships were significantly shifted upward by isoproterenol (p less than 0.05 or less); slope changes were variable. Pooled data from all dogs also showed a significant (p less than 0.001) upward shift in the pulmonary vascular V-P relationship regardless of which measure of distending pressure was used. These results suggest that beta-receptor stimulation by isoproterenol increases pulmonary vascular capacitance by increasing the unstressed volume.

Adrenergic beta-Agonists↗
PubMed1993

Effect of nifedipine on splanchnic and pulmonary vascular capacitance.

This study examines the hypothesis that nifedipine may increase splanchnic vascular capacitance and thus change the distribution of blood between the splanchnic and pulmonary circulation in heart failure patients. Relative regional blood volumes were determined by equilibrium blood pool scintigraphy during a 10 min baseline period and for 30 min after nifedipine 20 mg sublingually, with simultaneous recordings of systemic and pulmonary arterial pressures, hepatic venous wedge pressure, and cardiac output. Eight patients with ischaemic heart failure received nifedipine. Four patients served as controls. Nifedipine reduced mean arterial pressure and systemic vascular resistance in every patient. There were no significant changes in the relative blood volumes of the intestinal, hepatic, or splenic regions or in hepatic venous wedge pressure (reflecting portal venous pressure), suggesting unchanged splanchnic vascular pressure-volume relationship. Nifedipine caused a 6.3 +/- 1.0% increase in relative pulmonary blood volume and a slight increase in pulmonary vascular distending pressure from 16.1 +/- 2.9 mmHg to 17.5 +/- 2.8 mmHg (P < 0.05), suggesting that the increase in pulmonary blood volume was passively mediated. In conclusion, nifedipine did not change splanchnic vascular capacitance, but caused a small increase in pulmonary blood volume, which probably was a passive response to increased distending pressure.

Adult↗
PubMed1995

Vascular capacitance and cardiac output in pacing-induced canine models of acute and chronic heart failure.

The relationship between stressed and total blood volume, total vascular capacitance, central blood volume, cardiac output (CO), and pulmonary capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in anesthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2-6 weeks (average 24 +/- 2 days). Total vascular compliance and capacitance were calculated from the mean circulatory filling pressure (Pmcf) during transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodilution. Central (heart and lung) vascular capacitance was estimated from the plot of Ppcw against CBV. Acute volume loading without RRVP increased capacitance and CO, whereas after volume loading with RRVP, capacitance and CO were unaltered from baseline. Chronic RRVP reduced capacitance and CO. All interventions, volume +/- RRVP or chronic RRVP, increased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increased when stressed and unstressed blood volumes increased proportionately as during volume loading alone. When CO was reduced and Ppcw increased, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capacitance.

Acute Disease↗
PubMed1989

Vascular capacitance and reversal of 2-kidney, 1-clip hypertension in rats.

Vascular capacitance was studied in conscious early-phase (less than 6 wk) 2-kidney, 1-clip (2K, 1C) hypertension and compared with sham-clipped control rats. Two other groups of 2K, 1C rats were studied before and 6 h after unclipping or a sham operation. Mean circulatory filling pressure (MCFP) was measured during a brief circulatory arrest caused by inflation of a right atrial balloon. Blood volume (BV) was determined from plasma volume (125I-labeled albumin) and hematocrit. MCFP was measured at resting BV and after rapid BV changes. Vascular compliance was derived from the MCFP-BV curve. Hypertensive 2K, 1C rats had an increase in hematocrit (46 +/- 1.3 vs. 42 +/- 0.4%, P less than 0.01) and no difference in BV compared with controls. MCFP was increased (8.6 +/- 1.0 vs. 7.2 +/- 0.2 mmHg, P less than 0.01) with no difference in compliance, indicating decreased unstressed vascular volume in the 2K, 1C group. After unclipping, there was a significant fall in mean arterial pressure to normal, with a fall in MCFP (8.14 +/- 0.32 to 6.78 +/- 0.11 mmHg, P less than 0.01), but there was no difference in BV or compliance compared with the 2K, 1C group, indicating an increase in unstressed vascular volume after unclipping. These studies for the first time show an important role for vascular capacitance in modulating the circulatory changes accompanying the fall in blood pressure in surgical reversal of 2K, 1C hypertension.

Animals↗
PubMed1998

Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity.

BACKGROUND: Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose of this study is to test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) the capacitance change produced by propofol is a result of an inhibition of sympathetic vasoconstrictor activity. METHODS: In 33 Wistar rats previously anesthetized with urethane and ketamine, vascular capacitance was examined before and after propofol infusion by measuring mean circulatory filling pressure (Pmcf). The Pmcf was measured during a brief period of circulatory arrest produced by inflating an indwelling balloon in the right atrium. Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group. The Pmcf was measured at a control state and 2 min after a bolus administration of 2, 10, and 20 mg/kg of propofol. RESULTS: The mean arterial pressure (MAP) was decreased by propofol dose-dependently in intact, hypovolemic, and SNS-block groups, but the decrease in MAP was less in the SNS-block group (-25%) than in the intact (-50%) and hypovolemic (-61%) groups. In the SNS-block + NA group, MAP decreased only at 20 mg/kg of propofol (-18%). The Pmcf decreased in intact and hypovolemic groups in a dose-dependent fashion but was unchanged in the SNS-block and SNS-block + NA groups. CONCLUSIONS: The results have provided two principal findings: (1) propofol decreases Pmcf dose-dependently, and (2) the decrease in Pmcf by propofol is elicited only when the sympathetic nervous system is intact, suggesting that propofol increases systemic vascular capacitance as a result of an inhibition of sympathetic nervous system.

Anesthetics, Intravenous↗
PubMed1987

Alteration of blood flow distribution and vascular capacitance during induced hypotension in deafferented dogs.

The effects of three hypotensive agents, sodium nitroprusside (SNP), nitroglycerin (NTG), and adenosine triphosphate (ATP), on blood flow distribution and vascular capacitance were examined in dogs anesthetized with sodium pentobarbital. To eliminate the modification by the baroreflex, carotid sinus was denervated and aortic and cardiopulmonary vagal fibers were sectioned. Total systemic circulation was divided into two parallel compartments, splanchnic (SP) and extra-splanchnic (ESP) vascular beds. Alteration of vascular capacitance was assessed by a change in systemic blood volume with constant cardiac output and constant venous pressure using a total heart-lung bypass. SNP- and ATP-induced hypotension caused blood flow redistribution from the SP to ESP beds, and this redistribution is greater (P less than 0.01) with ATP than that with SNP. In contrast, NTG-induced hypotension did not significantly cause redistribution. Systemic blood volume was increased during NTG- (10.4 +/- 2.2 ml/kg), and SNP-induced (4.8 +/- 1.1 ml/kg) hypotension. The increase by NTG was significantly greater (P less than 0.05) than that by SNP. In contrast, ATP-induced hypotension did not significantly change systemic blood volume. Since redistribution can result in a passive change in vascular capacitance, the differences in capacitance among SNP, NTG, and ATP can be explained in part by differences in redistribution of blood flow. Redistribution of blood flow from SP to ESP beds can increase venous return due to increasing the slope of the venous return curve. The results suggest that redistribution should be taken into consideration in evaluating the hemodynamic changes during induced hypotension.

Adenosine Triphosphate↗
PubMed1990

Role of beta-adrenergic agonists in the control of vascular capacitance.

The role of beta-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 micrograms.min-1.kg-1), or isoproterenol (2.0 micrograms.min-1.kg-1), or histamine (4 micrograms.min-1.kg-1), or a combination of histamine and isoproterenol. Norepinephrine (an alpha- and beta 1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the beta-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.

Adrenergic beta-Agonists↗