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.

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.

Possible equilibration of portal venous and central venous pressures during circulatory arrest

1993 ◽  
Vol 264 (1) ◽  
pp. H259-H261 ◽  
Author(s):  
R. Tabrizchi ◽  
S. L. Lim ◽  
C. C. Pang
Keyword(s):  
Circulatory Arrest ◽  
Venous Pressure ◽  
Filling Pressure ◽  
Intravenous Bolus ◽  
Ang Ii ◽  
Central Venous ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Anesthetized Rats ◽  
Total Body

The mean circulatory filling pressure technique has been used to assess total body venous tone. It involves measuring central venous pressure (CVP) at 5-8 s following circulatory arrest. This study examines if CVP and portal venous pressure (PVP) equilibrate when circulation is stopped by inflating a balloon implanted in the right atrium. CVP and PVP were measured in the control condition and after intravenous bolus injections of norepinephrine (NE, 1.6 microgram/kg), angiotensin II (ANG II, 1.3 microgram/kg), and isoproterenol (Iso, 0.5 microgram/kg) in conscious and pentobarbital-anesthetized rats. In conscious rats, CVP was similar to PVP after circulatory arrest under conditions of normal, elevated, or reduced vascular tone. In anesthetized rats, CVP was similar to PVP in the control condition and after intravenous bolus injection of NE and Iso but was less than PVP after the administration of ANG II. Therefore, mean circulatory filling pressure may not fully reflect total body venous tone in anesthetized, surgically stressed rats.

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.

Decreased total venous capacity in Goldblatt hypertensive rats

1981 ◽  
Vol 240 (4) ◽  
pp. H487-H492 ◽  
Author(s):  
J. Yamamoto ◽  
N. C. Trippodo ◽  
A. A. MacPhee ◽  
E. D. Frohlich
Keyword(s):  
Circulatory Arrest ◽  
Filling Pressure ◽  
Right Atrial ◽  
Whole Body ◽  
Total Blood Volume ◽  
Hypertensive Rats ◽  
Total Blood ◽  
F Cells ◽  
Venous Capacity ◽  
Goldblatt Hypertension

Mean circulatory filling pressure (MCFP) and total blood volume (BV) were determined in conscious rats during the early, intermediate, and chronic phases of one-kidney, one-clip Goldblatt hypertension. MCFP was determined from arterial and venous plateau pressures during brief circulatory arrest, which was accomplished by inflating an indwelling right atrial balloon. BV as determined from plasma volume (125I-albumin), arterial hematocrit, and the F-cells factor. As compared with one-kidney sham groups, MCFP was significantly increased in one-kidney, one-clip Goldblatt hypertensive groups at 3, 14, and 28 days postclipping, whereas no significant differences in BV between hypertensive and normotensive groups were observed at any of these time periods. Total vascular compliance, estimated by measuring MCFP before and immediately after rapid BV changes, was significantly decreased in all one-kidney, one-clip Goldblatt hypertensive groups. These results indicate that venous constriction was increased and whole-body venous capacity was decreased in all three phases of one-kidney, one-clip Goldblatt hypertension studied. The mechanism leading to increased venous constriction in one-kidney, one-clip Goldblatt hypertension remains to be elucidated.

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

1989 ◽  
Vol 256 (2) ◽  
pp. H502-H507 ◽  
Author(s):  
M. E. Edmunds ◽  
G. I. Russell ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Circulatory Arrest ◽  
Filling Pressure ◽  
Right Atrial ◽  
Sham Operation ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
First Time

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.

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.

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