Increased cardiac output following occlusion of the descending thoracic aorta in dogs

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

Download Full-text

Limitations of thermodilution cardiac output measurements in the rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1984.246.6.h754 ◽

1984 ◽

Vol 246 (6) ◽

pp. H754-H760 ◽

Cited By ~ 2

Author(s):

B. E. Hayes ◽

J. A. Will ◽

W. C. Zarnstorff ◽

G. E. Bisgard

Keyword(s):

Cardiac Output ◽

Pulmonary Artery ◽

Right Ventricle ◽

Heat Loss ◽

Thoracic Aorta ◽

Vascular System ◽

Vena Cava ◽

Right Atrial ◽

Thermodilution Cardiac Output ◽

The Right

Heat loss from the vascular system could introduce an error in thermodilution cardiac output determinations. Cardiac output measured in the rat via the thermodilution technique following right atrial injection yielded different values (P less than 0.001), depending whether sampling was from the pulmonary artery (460 +/- 31 ml X min-1 X kg-1), right ventricle (311 +/- 19), or thoracic aorta (245 +/- 15). Recirculation errors could not account for the differences. Heat loss from the vascular system was measured from extravascular thermistors within both the thorax and the abdomen. These dilutions were 22-57% in peak height of aortic curves recorded at approximately the same location. Differences in calculated cardiac output between sampling sites could be attributed to rapid heat conduction directly from the right atrium and inferior vena cava to the thoracic aorta with progressive loss of indicator from both the right ventricle and pulmonary artery.

Download Full-text

Influence of the renal nerves on sodium excretion during progressive reductions in cardiac output

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.269.3.r678 ◽

1995 ◽

Vol 269 (3) ◽

pp. R678-R690 ◽

Cited By ~ 6

Author(s):

T. E. Lohmeier ◽

G. A. Reinhart ◽

H. L. Mizelle ◽

J. P. Montani ◽

R. Hester ◽

...

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Pulmonary Artery ◽

Arterial Pressure ◽

Sodium Excretion ◽

Pressure Control ◽

Atrial Pressure ◽

Right Atrial ◽

Renal Nerves ◽

Sodium Retention

The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.

Download Full-text

Interatrial shunt for chronic pulmonary hypertension: differential impact of low-flow vs. high-flow shunting

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00496.2008 ◽

2009 ◽

Vol 296 (3) ◽

pp. H639-H644 ◽

Cited By ~ 17

Author(s):

Andreas Zierer ◽

Spencer J. Melby ◽

Rochus K. Voeller ◽

Marc R. Moon

Keyword(s):

Pulmonary Hypertension ◽

Cardiac Output ◽

Superior Vena Cava ◽

Diastolic Pressure ◽

Superior Vena ◽

Vena Cava ◽

High Flow ◽

Low Flow ◽

Right Atrial ◽

Chronic Pulmonary Hypertension

The purpose of the present study was to determine for the first time the qualitative and quantitative impact of varying degrees of interatrial shunting on right heart dynamics and systemic perfusion in subjects with chronic pulmonary hypertension (CPH). Eight dogs underwent 3 mo of progressive pulmonary artery banding, following which right atrial and ventricular end-systolic and end-diastolic pressure-volume relations were calculated using conductance catheters. An 8-mm shunt prosthesis was inserted between the superior vena cava and left atrium, yielding a controlled model of atrial septostomy. Data were obtained 1) preshunt or “CPH”; 2) “Low-Flow” shunt; and 3) “High-Flow” shunt (occluding superior vena cava forcing all flow through the shunt). With progressive shunting, right ventricular pressure fell from 72 ± 19 mmHg (CPH) to 54 ± 17 mmHg (Low-Flow) and 47 ± 17 mmHg (High-Flow) ( P < 0.001). Cardiac output increased from 1.5 ± 0.3 l/min at CPH to 1.8 ± 0.4 l/min at Low-Flow (286 ± 105 ml/min, 15% of cardiac output; P < 0.001), but returned to 1.6 ± 0.3 l/min at High-Flow (466 ± 172 ml/min, 29% of cardiac output; P = 0.008 vs. Low-Flow, P = 0.21 vs. CPH). There was a modest rise in systemic oxygen delivery from 252 ± 46 ml/min at CPH to 276 ± 50 ml/min at Low-Flow ( P = 0.07), but substantial fall to 222 ± 50 ml/min at High-Flow ( P = 0.005 vs. CPH, P < 0.001 vs. Low-Flow). With progressive shunting, bichamber contractility did not change ( P = 0.98), but the slope of the right atrial end-diastolic pressure volume relation decreased ( P < 0.04), consistent with improved compliance. This study demonstrated that Low-Flow interatrial shunting consistently improved right atrial mechanics and systemic perfusion in subjects with CPH, while High-Flow exceeded an “ideal shunt fraction”.

Download Full-text

Comparative effects of arachidonic acid, bisenoic prostaglandins, and an endoperoxide analog on the canine pulmonary vascular bed

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y77-182 ◽

1977 ◽

Vol 55 (6) ◽

pp. 1369-1377 ◽

Cited By ~ 14

Author(s):

Philip J. Kadowitz ◽

Ernst W. Spannhake ◽

Stan Greenberg ◽

Larry P. Feigen ◽

Albert L. Hyman

Keyword(s):

Cardiac Output ◽

Arachidonic Acid ◽

Arterial Pressure ◽

Superior Vena Cava ◽

Right Atrium ◽

Pulmonary Arterial Pressure ◽

Superior Vena ◽

Vena Cava ◽

Aortic Pressure ◽

Pulmonary Arterial

The effects of bolus injections of the postaglandin precursor, arachidonic acid, and PGD2, PGF2α, PGE2, and the PGH2 analog ((15S)-hydroxyl-9α,11α(epoxymethano)-prosta-5Z-dienoic acid) were compared on the pulmonary circulation in the intact spontaneously breathing pentobarbital-anesthetized dog. Arachidonic acid increased pulmonary arterial pressure, decreased aortic pressure, and increased cardiac output when injected into the superior vena cava or right atrium. PGE2, like arachidonic acid, increased pulmonary arterial pressure and cardiac output and decreased aortic pressure, whereas PGF2α and PGD2 increased pulmonary arterial pressure but did not affect cardiac output or aortic pressure when injected into the superior vena cava or right atrium. The PGH2 analog increased pulmonary arterial pressure and to a lesser extent, aortic pressure, without affecting cardiac output. None of these substances changed left atrial or right atrial pressure. The cardiopulmonary effects of arachidonic acid were blocked by indomethacin whereas the rise in pulmonary arterial pressure in response to the bisenoic prostaglandins and the analog were enhanced by the cyclooxygenase inhibitor. These data suggest that the increase in pulmonary vascular resistance in response to arachidonic acid may be due to conversion of the precursor into vasoactive intermediates and products such as bisenoic prostaglandins whereas the decrease in systemic vascular resistance is probably due to the formation of PGE2 and other peripheral vasodilator substances.

Download Full-text

What Goes Around Comes Around—Venous Return

Just Enough Physiology ◽

10.1093/med/9780199797790.003.0006 ◽

2011 ◽

pp. 48-54

Author(s):

James R. Munis

Keyword(s):

Cardiac Output ◽

Steady State ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Cardiovascular System ◽

Venous Return ◽

Atrial Pressure ◽

Right Atrial ◽

Interconnected System ◽

The Mean

By its nature, circulatory physiology is also susceptible to circular reasoning because every part of an interconnected system is affected by, and affects, every other part. If we're not careful, we end up saying things like ‘venous return equals cardiac output’ when, in the steady state, that is true by definition and nothing new is gained. If we grant that right atrial pressure (PRA) is the ‘downstream’ pressure for venous return, then it follows that PRA should be inversely related to venous return (and therefore, to cardiac output). If we simply apply Ohm's law to the cardiovascular system, we forget that the mean arterial pressure not only contributes to venous return but also is sustained by venous return. If venous return fails for any other reason (unrelated to arterial pressure), so too will mean arterial pressure eventually fail.

Download Full-text

Hemodynamic studies in DOCA-salt hypertensive rats after opening of an arteriovenous fistula

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.6.h1802 ◽

1992 ◽

Vol 262 (6) ◽

pp. H1802-H1808 ◽

Cited By ~ 1

Author(s):

M. Huang ◽

R. L. Hester ◽

A. C. Guyton ◽

R. A. Norman

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Atrial Pressure ◽

Right Atrial ◽

Right Atrial Pressure ◽

Hypertensive Rats

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6–8 wk. At the end of 10–12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Systemic hemodynamic effects of leukotrienes C4 and D4 in the rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.244.4.h628 ◽

1983 ◽

Vol 244 (4) ◽

pp. H628-H633 ◽

Cited By ~ 1

Author(s):

M. A. Pfeffer ◽

J. M. Pfeffer ◽

R. A. Lewis ◽

E. Braunwald ◽

E. J. Corey ◽

...

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Right Atrial ◽

Moderate Pressure ◽

Hemodynamic Effects ◽

Systemic Hemodynamic ◽

Leukotriene D4

Although local administration of the sulfidopeptide leukotrienes into cutaneous and coronary vascular beds indicates that these naturally occurring metabolites of arachidonic acid are vasoconstrictors, their systemic administration has produced both pressor and depressor responses. The systemic hemodynamic effects of intravenous leukotriene C4 (LTC4) and leukotriene D4 (LTD4) were assessed in ether-anesthetized rats and compared with the effects produced by equimolar doses (2 X 10(-10) to 4 X 10(-8) mol/kg) of norepinephrine and angiotensin. Mean arterial pressure, right atrial pressure, and cardiac output (electromagnetic flowmetry) were recorded during bolus administrations of these vasoactive compounds. LTC4 and LTD4 had similar hemodynamic effects that were characterized by moderate pressure elevations produced by dose-dependent increases in total peripheral resistance, since cardiac output declined. Although the peak mean arterial pressure levels produced by LTC4 and LTD4 (135 +/- 7 and 129 +/- 5 mmHg, respectively) were less than those by norepinephrine (157 +/- 3 mmHg) and angiotensin (174 +/- 5 mmHg), the peak total peripheral resistance values of LTC4 and LTD4 (2.23 +/- 0.32 and 1.86 +/- 0.17 mmHg X ml-1 X min-1, respectively) were between those of the well-known vasopressors, norepinephrine (1.50 +/- 0.09) and angiotensin (2.72 +/- 0.41). The pressor response to LTC4 and LTD4 was less marked than that to norepinephrine and to angiotensin because of the concomitant reduction in cardiac output. These results indicate that LTC4 and LTD4 are systemic vasoconstrictors with potencies similar to those of norepinephrine and angiotensin.

Download Full-text

Effects of ANP-(95-126) in dogs before and after induction of heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.6.h1643 ◽

1990 ◽

Vol 259 (6) ◽

pp. H1643-H1648

Author(s):

G. A. Riegger ◽

D. Elsner ◽

W. G. Forssmann ◽

E. P. Kromer

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Right Atrial ◽

Peripheral Vascular ◽

Before And After ◽

Pulmonary Arterial

In conscious dogs with and without congestive heart failure, we investigated hemodynamic, hormonal, and renal effects of a new natriuretic peptide [ANP-(95-126)]. Unlike ANP-(99-126), which is secreted in the heart and rapidly inactivated in the kidney, ANP-(95-126) most likely originates from the kidney and is not destroyed by proteolysis in membrane preparations of kidney cortex. In healthy animals intravenous ANP-(95-126) significantly decreased mean arterial pressure, cardiac output, stroke volume, and right atrial pressure and increased heart rate without changing mean pulmonary arterial pressure and total peripheral vascular resistance. In dogs with congestive heart failure, ANP-(95-126) showed no effects on mean arterial pressure, cardiac output, stroke volume, and peripheral vascular resistance but reduced right atrial pressure and pulmonary arterial pressure. Both, in dogs before and after the induction of heart failure, the new peptide led to a significant increase of urine flow and sodium and chloride excretion. In healthy dogs there were indirect indications for a small inhibitory effect on renin and aldosterone secretion. Thus, in contrast to the considerable attenuation of renal effects of ANP-(99-126) in heart failure, the efficacy of ANP-(95-126) on renal excretory function is well preserved, which may be because of the lack of proteolytic degradation in the kidney. These results suggest that ANP-(95-126) may have clinical implications for the treatment of patients with congestive heart failure.

Download Full-text

Single-Patch Fold-Back Technique for Augmentation of the Superior Vena Cava in Sinus Venosus Atrial Septal Defect Associated with Partial Anomalous Pulmonary Venous Return

The Heart Surgery Forum ◽

10.1532/hsf98.2014433 ◽

2015 ◽

Vol 17 (6) ◽

pp. 282

Author(s):

Suguru Ohira ◽

Kiyoshi Doi ◽

Takeshi Nakamura ◽

Hitoshi Yaku

Keyword(s):

Atrial Septal Defect ◽

Superior Vena Cava ◽

Septal Defect ◽

Venous Return ◽

Superior Vena ◽

Pulmonary Veins ◽

Vena Cava ◽

Sinus Venosus ◽

Right Atrial ◽

Anomalous Pulmonary Venous Return

Sinus venosus atrial septal defect (ASD) is usually associated with partial anomalous pulmonary venous return (PAPVR) of the right pulmonary veins to the superior vena cava (SVC), or to the SVC-right atrial junction. Standard procedure for repair of this defect is a patch roofing of the sinus venosus ASD and rerouting of pulmonary veins. However, the presence of SVC stenosis is a complication of this technique, and SVC augmentation is necessary in some cases. We present a simple technique for concomitant closure of sinus venosus ASD associated with PAPVR and augmentation of the SVC with a single autologous pericardial patch.

Download Full-text