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.

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.

Measurement of mean circulatory filling pressure and vascular compliance in domestic pigs

1990 ◽  
Vol 258 (6) ◽  
pp. H1925-H1932 ◽  
Author(s):  
R. I. Ogilvie ◽  
D. Zborowska-Sluis ◽  
B. Tenaschuk
Keyword(s):  
Cardiac Arrest ◽  
Circulatory Arrest ◽  
Filling Pressure ◽  
Right Atrial ◽  
Base Line ◽  
Pentobarbital Sodium ◽  
Closed Chest ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance ◽  
Venous Circulation

To measure mean circulatory filling pressure (Pmcf), a balloon was placed in the right atrium of seven pentobarbital sodium-anesthetized open-chest pigs for transient occlusion of flow combined with mechanical transfer of blood from the arterial to the venous circulation. Equilibration occurred within 6-8 s at a pressure at 12.3 +/- 0.3 (SE) mmHg after a 2.9 +/- 0.2 ml/kg transfer of blood. In another group of pentobarbital sodium-anesthetized closed-chest pigs, acetylcholine (ACh) was used to induce cardiac arrest. The Pmcf was 11.6 +/- 1.0 mmHg in the 7:17 pigs that arrested for 6-8 s. In four isoflurane-anesthetized closed-chest pigs, the Pmcf was 12.0 +/- 1.0 mmHg after terminal cardiac arrest induced by KCl. The pressure gradient for venous return [Pmcf--right atrial pressure (Pra)] averaged 5.9 +/- 0.2 mmHg. Total vascular compliance estimated from plots of Pmcf at base line, 5, and 10 ml/kg increases in circulating volume was 2.1 +/- 0.3 and 3.5 +/- 0.9 ml.kg-1.mmHg-1 in the balloon and ACh groups, respectively compared with 2.8 +/- 0.4 ml.kg-1.mmHg-1 using a volume infusion-withdrawal method without circulatory arrest. The use of ACh for the estimate of Pmcf in the pig is not recommended because of failure to consistently induce circulatory arrest and probable failure to achieve sufficient equilibrium of vascular pressures 6-8 s postarrest when it occurs.

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.

Vascular compliance and mean circulatory filling pressure in trout: effects of ACE inhibition

1995 ◽  
Vol 268 (5) ◽  
pp. H1814-H1820 ◽  
Author(s):  
Y. Zhang ◽  
E. Jenkinson ◽  
K. R. Olson
Keyword(s):  
Blood Volume ◽  
Ace Inhibition ◽  
Filling Pressure ◽  
Whole Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance ◽  
Cardiac Fibrillation ◽  
Arterial Blood ◽  
Zero Flow

Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (PDA) and sinus venosus (PSV) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (approximately 5 s) dropped PDA and increased PSV (equals MCFP). MCFP in normovolemic trout (4.8 +/- 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml.mmHg-1.kg body wt-1, respectively). USV was 13.3 ml/kg body wt (approximately 45% of BV). ACE inhibition reduced PDA in unfibrillated trout at all BV and reduced PDA in fibrillated fish at BV > or = 80%. ACE inhibition did not affect PSV, MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (delta PF0) was greatest at 100% BV (8.2 +/- 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in delta PF0 during ACE inhibition is due to a decrease in arteriolar resistance.

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)

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.

scholarly journals Understanding Guyton's venous return curves

2011 ◽  
Vol 301 (3) ◽  
pp. H629-H633 ◽  
Author(s):  
Daniel A. Beard ◽  
Eric O. Feigl
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Venous Return ◽  
Systemic Circulation ◽  
Back Pressure ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Simultaneous Increase ◽  
Venous Circulation

Based on observations that as cardiac output (as determined by an artificial pump) was experimentally increased the right atrial pressure decreased, Arthur Guyton and coworkers proposed an interpretation that right atrial pressure represents a back pressure restricting venous return (equal to cardiac output in steady state). The idea that right atrial pressure is a back pressure limiting cardiac output and the associated idea that “venous recoil” does work to produce flow have confused physiologists and clinicians for decades because Guyton's interpretation interchanges independent and dependent variables. Here Guyton's model and data are reanalyzed to clarify the role of arterial and right atrial pressures and cardiac output and to clearly delineate that cardiac output is the independent (causal) variable in the experiments. Guyton's original mathematical model is used with his data to show that a simultaneous increase in arterial pressure and decrease in right atrial pressure with increasing cardiac output is due to a blood volume shift into the systemic arterial circulation from the systemic venous circulation. This is because Guyton's model assumes a constant blood volume in the systemic circulation. The increase in right atrial pressure observed when cardiac output decreases in a closed circulation with constant resistance and capacitance is due to the redistribution of blood volume and not because right atrial pressure limits venous return. Because Guyton's venous return curves have generated much confusion and little clarity, we suggest that the concept and previous interpretations of venous return be removed from educational materials.

Vascular pressure-volume relationships in pregnant and estrogen-treated guinea pigs

1989 ◽  
Vol 257 (5) ◽  
pp. R1205-R1211 ◽  
Author(s):  
L. E. Davis ◽  
A. R. Hohimer ◽  
G. D. Giraud ◽  
M. S. Paul ◽  
M. J. Morton
Keyword(s):  
Blood Volume ◽  
Guinea Pigs ◽  
Circulatory Arrest ◽  
Right Atrial ◽  
Blood Volume Expansion ◽  
Rapid Ventricular Pacing ◽  
The Difference ◽  
Unanesthetized Animals ◽  
The Relationship ◽  
Estrogen Administration

We investigated the relationship between mean circulatory filling pressure (MCFP) and blood volume in nonpregnant (NP), estrogen-treated (E), and pregnant (P) guinea pigs. Reversible circulatory arrest was produced by rapid ventricular pacing or acetylcholine in unanesthetized animals remote from surgery. MCFP (mmHg) was higher for E (7.1 +/- 0.3) than for NP (5.8 +/- 0.5) or P (5.3 +/- 0.4). The gradient for venous return, the difference between MCFP and right atrial pressure (mmHg), did not differ in NP- (6.0 +/- 0.5), P- (5.8 +/- 0.5), or E- (5.8 +/- 0.4) treated animals. Capacitance, the blood volume (ml/kg) at an MCFP of 6 mmHg, was increased in P (84 +/- 6) and E (89 +/- 7), compared with NP (64 +/- 5) animals. Compliance, the ratio of the change in volume to change in pressure in the range of 6-12 mmHg (ml.kg-1.mmHg-1), was greater in P (4.4 +/- 0.3) than NP (3.5 +/- 0.3) animals. Hexamethonium blockade did not affect MCFP, capacitance, or compliance. We conclude that the effect of blood volume expansion on the circulation in pregnancy cannot be predicted from knowledge of MCFP-blood volume relationships in the nonpregnant animal, because capacitance and compliance are altered. Estrogen administration to nonpregnant animals reproduces some of these effects.

Hindlimb unweighting affects rat vascular capacitance function

2001 ◽  
Vol 281 (3) ◽  
pp. H1170-H1177 ◽  
Author(s):  
Stacey L. Dunbar ◽  
Laleh Tamhidi ◽  
Dan E. Berkowitz ◽  
Artin A. Shoukas
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Arterial Compliance ◽  
Filling Pressure ◽  
Right Atrial ◽  
Orthostatic Stress ◽  
Venous Compliance ◽  
Reservoir Volume ◽  
Venous Filling ◽  
And Control

Microgravity is associated with an impaired stroke volume and, therefore, cardiac output response to orthostatic stress. We hypothesized that a decreased venous filling pressure due to increased venous compliance may be an important contributing factor in this response. We used a constant flow, constant right atrial pressure cardiopulmonary bypass procedure to measure total systemic vascular compliance (CT), arterial compliance (CA), and venous compliance (CV) in seven control and seven 21-day hindlimb unweighted (HLU) rats. These compliance values were calculated under baseline conditions and during an infusion of 0.2 μg · kg−1 · min−1norepinephrine (NE). The change in reservoir volume, which reflects changes in unstressed vascular volume (ΔV0) that occurred upon infusion of NE, was also measured. CT and CV were larger in HLU rats both at baseline and during the NE infusion ( P < 0.05). Infusion of NE decreased CT and CV by ∼20% in both HLU and control rats ( P < 0.01). CA was also significantly decreased in both groups of rats by NE ( P < 0.01), but values of CA were similar between HLU and control rats both at baseline and during the NE infusion. Additionally, the NE-induced ΔV0 was attenuated by 53% in HLU rats compared with control rats ( P < 0.05). The larger CV and attenuated ΔV0 in HLU rats could contribute to a decreased filling pressure during orthostasis and thus may partially underlie the mechanism leading to the exaggerated fall in stroke volume and cardiac output seen in astronauts during an orthostatic stress after exposure to microgravity.

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