Role of β-adrenergic agonists in the control of vascular capacitance

1990 ◽  
Vol 68 (5) ◽  
pp. 575-585 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Filling Pressure ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Central Venous ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance

The role of β-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 μg∙min−1∙kg−1), or isoproterenol (2.0 μg∙min−1∙kg−1), or histamine (4 μg∙min−1∙kg−1), or a combination of histamine and isoproterenol. Norepinephrine (an α- and β1-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 β-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.Key words: β-adrenergic agonists, vascular capacitance, mean circulatory filling pressure, isoproterenol, histamine, liver sphincters.

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

1990 ◽  
Vol 68 (3) ◽  
pp. 384-391 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

Mean circulatory filling pressure: its meaning and measurement

1993 ◽  
Vol 74 (2) ◽  
pp. 499-509 ◽  
Author(s):  
C. F. Rothe
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Muscle Tone ◽  
Rapid Change ◽  
Circulatory System ◽  
Filling Pressure ◽  
The Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

The volume-pressure relationship of the vasculature of the body as a whole, its vascular capacitance, requires a measurement of the mean circulatory filling pressure (Pmcf). A change in vascular capacitance induced by reflexes, hormones, or drugs has physiological consequences similar to a rapid change in blood volume and thus strongly influences cardiac output. The Pmcf is defined as the mean vascular pressure that exists after a stop in cardiac output and redistribution of blood, so that all pressures are the same throughout the system. The Pmcf is thus related to the fullness of the circulatory system. A change in Pmcf provides a uniquely useful index of a change in overall venous smooth muscle tone if the blood volume is not concomitantly changed. The Pmcf also provides an estimate of the distending pressure in the small veins and venules, which contain most of the blood in the body and comprise most of the vascular compliance. Thus the Pmcf, which is normally independent of the magnitude of the cardiac output, provides an estimate of the upstream pressure that determines the rate of flow returning to the heart.

Effects of nifedipine and captopril on vascular capacitance of ganglion-blocked anesthetized dogs

1990 ◽  
Vol 68 (3) ◽  
pp. 431-438 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Filling Pressure ◽  
Right Atrial ◽  
Central Blood Volume ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Blood Volumes

The hemodynamic effects of nifedipine and captopril at doses producing similar reductions in arterial pressure were studied in pentobarbital- anesthetized ventilated dogs after splenectomy during ganglion blockade with hexamethonium. Mean circulatory filling pressure (Pmcf) was determined during transient circulatory arrest induced by acetylcholine at baseline circulating blood volumes and after increases of 5 and 10 mL/kg. Central blood volumes (pulmonary artery to aortic root) were determined from transit times, and separately determined cardiac outputs (right atrium to pulmonary artery) were estimated by thermodilution. Nifedipine (n = 5) increased Pmcf at all circulating blood volumes and reduced total vascular capacitance without a change in total vascular compliance. Central blood volume, right atrial pressure, and cardiac output were increased with induced increases in circulating blood volume. In contrast, captopril (n = 5) did not alter total vascular capacitance, central blood volume, right atrial pressure, or cardiac output at baseline or with increased circulating volume. Thus, at doses producing similar reductions in arterial pressure, nifedipine but not captopril increased venous return and cardiac output in ganglion-blocked dogs.Key words: mean circulatory filling pressure, vascular compliance, vascular capacitance, nifedipine, captopril.

Alpha 1- and alpha 2-adrenoceptor stimulation: changes in venous capacitance in intact dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1071-H1078
Author(s):  
C. P. Appleton ◽  
R. W. Lee ◽  
G. V. Martin ◽  
M. Olajos ◽  
S. Goldman
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Aortic Pressure ◽  
Filling Pressure ◽  
Venous Capacitance ◽  
Mean Circulatory Filling Pressure ◽  
Control Value ◽  
Circulatory Effects ◽  
Mean Aortic Pressure ◽  
Effective Vascular Compliance

The peripheral circulatory effects of alpha 1-adrenoceptor stimulation with methoxamine hydrochloride were compared with those of alpha 2-stimulation with UK 14304-18 in 12 intact dogs. Doses of each agent were infused to increase systemic vascular resistance and arterial pressure 50 and then 100% above control. Heart rate was controlled with atropine. At the higher dose, methoxamine increased mean aortic pressure (PAo) from a control of 77.3 +/- 1.6 to 152.9 +/- 3.2 mmHg, mean circulatory filling pressure (MCFP) from 8.0 +/- 0.4 to 13.3 +/- 1.3 mmHg, and central blood volume (CBV) from 21.3 +/- 1.1 to 25.9 +/- 1.5 ml X kg-1, whereas cardiac output did not change. UK 14304-18 increased PAo from 78.1 +/- 2.6 to 148.9 +/- 2.7 mmHg, MCFP from 7.9 +/- 0.4 to 10.6 +/- 0.4 mmHg, and CBV from 21.0 +/- 1.1 to 24.1 +/- 1.5 ml X kg-1, whereas cardiac output decreased from 151.7 +/- 9.4 to 126.3 +/- 5.8 ml X kg-1 X min-1. Mean circulatory filling pressure and CBV were higher with methoxamine than with UK 14304-18. Effective vascular compliance, determined by serial measurements of MCFP during ganglionic blockade after rapid changes in blood volume, decreased from a control value of 1.9 +/- 0.1 to 1.3 +/- 0.3 ml X mmHg-1 X kg-1 with methoxamine, but did not change with UK 14304-18 (1.9 +/- 0.1 ml X mmHg-1 X kg-1). At any given change in blood volume, there was a higher MCFP with alpha 1-stimulation compared with alpha 2-stimulation. Both agents decreased unstressed vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of pregnancy on mean systemic filling pressure and the cardiac function curve in guinea pigs

1992 ◽  
Vol 70 (5) ◽  
pp. 669-674 ◽  
Author(s):  
S. C. Cha ◽  
G. W. Aberdeen ◽  
B. S. Nuwayhid ◽  
E. W. Quillen Jr.
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Cardiac Function ◽  
Blood Volume ◽  
Guinea Pigs ◽  
Venous Return ◽  
Filling Pressure ◽  
Right Atrial ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance

To assess the degree of circulatory fullness and to evaluate the influence of peripheral and cardiac factors in the regulation of cardiac output during pregnancy, the following studies were conducted using pentobarbital-anesthetized, open-chest nonpregnant and late term pregnant guinea pigs. Mean circulatory filling pressure was taken as the equilibrium pressure when the pulmonary artery was constricted. Total vascular compliance was assessed by ±5-mL changes in blood volume performed while this constriction was maintained. A separate group of guinea pigs was prepared with a pulmonary artery electromagnetic flow probe and right atrial catheter. Rapid infusion of saline was used to increase right atrial pressure while the cardiac output was determined. Pregnancy was characterized by the following changes relative to nonpregnant controls: 51Cr-labelled RBC blood volume increased from 55 ± 3 to 67 ± 3 mL/kg; mean circulatory filling pressure increased from 7.1 ± 0.2 to 8.0 ± 0.5 mmHg (1 mmHg = 133.322 Pa); right atrial pressure decreased from 3.4 ± 0.2 to 2.1 ± 0.3 mmHg; and cardiac output increased from 71.8 ± 3.9 to 96.8 ± 3.3 mL∙min−1∙kg−1. Total vascular compliance was not changed (2.1 ± 0.1 mL∙kg−1∙mmHg−1) and most of the expanded blood volume was accommodated as unstressed volume. The cardiac function curve was shifted upwards in pregnant animals. The resistance to venous return, as determined from the slope of the venous return curves, was not changed. These data suggest that the circulation of the pregnant guinea pig is slightly overfilled. The pressure gradient for venous return was increased, but a more important contribution to the increased levels of cardiac output is made by the increase in cardiac pumping ability.Key words: blood volume, mean circulatory filling pressure, vascular compliance, venous return.

Role of postural status in the nocturnal hemodynamic patterns of nonhuman primates

1993 ◽  
Vol 74 (4) ◽  
pp. 1684-1688 ◽  
Author(s):  
B. T. Engel ◽  
M. I. Talan ◽  
P. H. Chew
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Total Peripheral Resistance ◽  
Nonhuman Primates ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Central Venous ◽  
Hemodynamic Pattern ◽  
Biologic Effect

We compared the nocturnal hemodynamic patterns of seven tethered monkeys (Macaca mulatta) with those of seven chaired animals to determine whether the overnight changes are comparable in the two conditions. In both groups, we found a consistent hemodynamic pattern characterized by an overnight fall in cardiac output and central venous pressure and a rise in total peripheral resistance that maintained blood pressure homeostasis. The pattern of overnight change occurred despite major differences in response levels: cardiac output and central venous pressure were significantly elevated, and total peripheral resistance was significantly reduced at all times (from 1800 to 1200 h the following day) in the chaired animals relative to the tethered animals. This difference was probably due to an expanded plasma volume in the chaired animals, because stroke volume was also significantly elevated. Because the nocturnal hemodynamic pattern occurred under both conditions, it is likely that it is a stable biologic effect, which is probably related to an overnight loss in fluid volume that is not replaced in animals that sleep throughout the night.

Effects of freshwater and saltwater adaptation and dietary salt on fluid compartments, blood pressure, and venous capacitance in trout

2008 ◽  
Vol 294 (3) ◽  
pp. R1061-R1067 ◽  
Author(s):  
Kenneth R. Olson ◽  
Todd M. Hoagland
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Extracellular Fluid ◽  
Filling Pressure ◽  
Salt Balance ◽  
Salt Loading ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Fluid Compartments ◽  
The Relationship

Trout are of interest in defining the relationship between fluid and salt balance on cardiovascular function because they thrive in freshwater (FW; volume loading, salt depleting), saltwater (SW; volume depleting, salt loading), and FW while fed a high-salt diet (FW-HS; volume and salt loading). The effects of chronic (>2 wk) adaptation to these three protocols on blood volume (51Cr red cell space), extracellular fluid volume (99mTc-diethylene triaminepenta-acetic acid space), arterial (dorsal aortic; PDA) and venous (ductus Cuvier; Pven) blood pressure, mean circulatory filling pressure (zero-flow Pven), and vascular capacitance were examined in the present study on unanesthetized rainbow trout. Blood volume, extracellular fluid volume, PDA, Pven, and mean circulatory filling pressure progressively increased in the order SW < FW < FW-HS. Vascular capacitance in SW fish appeared to be continuous with the capacitance curve of FW fish and reflect a passive volume-dependent unloading of the venous system of FW fish. Vascular capacitance curves for FW-HS fish were displaced upward and parallel to those of FW fish, indicative of an active increase in unstressed blood volume without any change in vascular compliance. These studies are the first in any vertebrate to measure the relationship between fluid compartments and cardiovascular function during independent manipulation of volume and salt balance, and they show that volume, but not salt, balance is the primary determinant of blood pressure in trout. They also present a new paradigm with which to investigate the relative contributions of water and salt balance in cardiovascular homeostasis.

Essential role of mean circulatory filling pressure in salt-induced hypertension

1979 ◽  
Vol 236 (1) ◽  
pp. R40-R47 ◽  
Author(s):  
R. D. Manning ◽  
T. G. Coleman ◽  
A. C. Guyton ◽  
R. A. Norman ◽  
R. E. McCaa
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Isotonic Saline ◽  
Filling Pressure ◽  
Initial Increase ◽  
Experimental Hypertension ◽  
Base Line ◽  
Plasma Aldosterone Concentration ◽  
Salt Loading ◽  
Mean Circulatory Filling Pressure

Experimental hypertension was produced in nine dogs by continuously infusing isotonic saline after renal mass had been surgically reduced to approximately 30% normal. Data were collected during 8 days of base-line measurements and 13 days of saline infusion to determine the cause of the initial increase in cardiac output observed in this type of hypertension and to measure other variables possibly important in the pathogenesis of hypertension. During the infusion period, these dogs demonstrated an increase in arterial pressure to hypertensive levels, transient increases in blood volume, sodium space, and cardiac output, initially depressed then subsequently elevated total peripheral resistance, and decreases in plasma renin activity and plasma aldosterone concentration. The mean circulatory filling pressure increased 4.7 Torr by day 3 and was still elevated 2 Torr at the end of the 2nd wk of infusion. We conclude that the initial increase in cardiac output in salt-loading hypertension is due to elevated fluid volumes and the associated increase in mean circulatory filling pressure.

Vascular capacitance responses to hypercapnia of the vascularly isolated head

1986 ◽  
Vol 251 (1) ◽  
pp. H164-H170 ◽  
Author(s):  
M. L. Gaddis ◽  
C. L. MacAnespie ◽  
C. F. Rothe
Keyword(s):  
Peripheral Resistance ◽  
Systemic Circulation ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Whole Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Carotid Bodies ◽  
The Brain ◽  
Stimulation Of

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.

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