Effect of varying coronary perfusion on ventricular function in isolated dog hearts

1964 ◽  
Vol 207 (3) ◽  
pp. 683-690 ◽  
Author(s):  
N. M. Buckley ◽  
E. P. Porter ◽  
L. A. Jedeikin
Keyword(s):  
Oxygen Consumption ◽  
Ventricular Function ◽  
Oxygen Content ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Arterial Oxygen ◽  
Coronary Perfusion ◽  
Stroke Work ◽  
Arterial Oxygen Content

The effects of coronary perfusion on ventricular function have been studied in isolated ventricle preparations working under different conditions. Coronary flow, oxygen consumption, ventricular stroke work, rate of ventricular pressure change during isovolumetric contraction (dPC), and diastolic ventricular pressure (DVPm) and pressure/inflow ratio were determined. Maintenance of coronary flow and oxygen consumption in 5 experiments did not prevent irreversible changes in DVPm, stroke work, and dPC when the right ventricle was acutely overloaded. These ventricles did not accumulate water. Decreasing coronary perfusion pressure at constant arterial oxygen content in 11 experiments led to inconsistent changes in DVPm, stroke work and dPC. Decreasing arterial oxygen content at constant coronary perfusion pressure in 10 experiments led to increased DVPm but inconsistent changes in stroke work and dPC. There was an inverse relationship between DVPm and oxygen consumption in the variable perfusion experiments, but not in the overloading experiments. Ventricular function did not change significantly with time in 6 experiments in which the conditions of workload and coronary perfusion were kept constant. It was concluded that irreversible changes in performance of acutely overloaded ventricles could be independent of coronary flow, myocardial water content, or duration of experiment.

Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion

1985 ◽  
Vol 249 (6) ◽  
pp. H1070-H1077 ◽  
Author(s):  
I. Y. Liang ◽  
C. E. Jones
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Adrenergic Blockade ◽  
Adrenergic Antagonist

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6–8 min of prazosin infusion (0.6–0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

Adrenal blood flow and secretory relationships during hypoxia in anesthetized dogs

1989 ◽  
Vol 257 (5) ◽  
pp. H1458-H1465 ◽  
Author(s):  
M. J. Breslow ◽  
T. D. Ball ◽  
C. F. Miller ◽  
H. Raff ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Oxygen Content ◽  
Adrenocorticotropic Hormone ◽  
Secretory Activity ◽  
Catecholamine Secretion ◽  
Arterial Oxygen ◽  
Vascular Effects ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs

To evaluate whether hypoxia-induced increases in adrenal cortical (CQ) and medullary (MQ) blood flow (radiolabeled microspheres) occur secondary to hypoxia-induced secretory activity, pentobarbital-anesthetized ventilated dogs were pretreated with dexamethasone (DEX) to prevent adrenocorticotropic hormone (ACTH) and corticosteroid secretory changes or underwent unilateral adrenal denervation to prevent adrenal catecholamine secretory responses. In nonsurgically stressed dogs, DEX completely prevented increases in ACTH or corticosteroid levels during reduction of arterial oxygen content to 8 vol% but had no effect on hypoxia-induced doubling of CQ. In dogs in which adrenal oxygen consumption (VO2) was measured, DEX reduced VO2 by 50% without altering CQ. Unilateral adrenal denervation prevented hypoxia-induced increases in adrenal catecholamine secretion and MQ but had no effect on the CQ response. These results suggest that hypoxia-induced medullary vasodilation is associated with adrenal catecholamine secretory activity but that increases in CQ occur independent of secretory activity and likely represent direct vascular effects of hypoxia.

scholarly journals Response of the Intact Canine Left Ventricle to Increased Afterload and Increased Coronary Perfusion Pressure in the Presence of Coronary Flow Autoregulation

Circulation ◽  
1999 ◽  
Vol 100 (14) ◽  
pp. 1562-1568 ◽  
Author(s):  
Mohanraj K. Karunanithi ◽  
Jason A. Young ◽  
Wally Kalnins ◽  
Scott Kesteven ◽  
Michael P. Feneley
Keyword(s):  
Left Ventricle ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion

Coronary pressure-flow autoregulation protects myocardium from pressure-induced changes in oxygen consumption

1994 ◽  
Vol 266 (6) ◽  
pp. H2359-H2368 ◽  
Author(s):  
X. J. Bai ◽  
T. Iwamoto ◽  
A. G. Williams ◽  
W. L. Fan ◽  
H. F. Downey
Keyword(s):  
Oxygen Consumption ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Coronary Perfusion ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Anesthetized Dogs ◽  
Induced Changes

Pressure-flow autoregulation minimizes changes in coronary blood flow (CBF) when coronary perfusion pressure (CPP) is altered. This investigation determined if autoregulation also minimizes CPP-induced changes in coronary vascular volume (CVV) and CVV-dependent changes in myocardial oxygen consumption (MVO2). In 11 anesthetized dogs, the left anterior descending coronary artery was cannulated, and responses to 20-mmHg changes in CPP were examined over a range of CPP from 60 to 180 mmHg. Changes in CPP had no significant effect on systemic hemodynamics or on left ventricular end-diastolic segment length, end-systolic segment length, or percent segment shortening. In hearts with effective pressure-flow autoregulation [closed-loop gain (GC) > 0.4], CVV increased 0.06%/mmHg change in CPP. For the same hearts, MVO2 increased 0.04%/mmHg change in CPP. In hearts with ineffective autoregulation (GC < 0.4), CVV increased 0.97%/mmHg (P < 0.001 vs. autoregulating hearts), and MVO2 increased 0.41%/mmHg (P < 0.001 vs. autoregulating hearts). MVO2 and CVV were correlated (r = 0.69, P < 0.0001) independently of autoregulatory capability, but only when autoregulation was poor and capacitance was elevated did CPP significantly affect MVO2. We conclude that pressure-flow autoregulation protects myocardium from CPP-induced changes in CVV, which in turn produces changes in oxygen consumption.

Effect of Aortic Distensibility on Coronary Flow: A 3D FSI Model of Aortic Valve With the Inclusion of Coronary Arteries

2011 ◽  
Author(s):  
Soroush Nobari ◽  
Rosaire Mongrain ◽  
Richard Leask ◽  
Raymond Cartier
Keyword(s):  
Coronary Flow ◽  
Aortic Wall ◽  
Perfusion Pressure ◽  
Aortic Distensibility ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Metabolic Demand ◽  
Calcific Aortic Stenosis ◽  
Pathological Conditions ◽  
Aortic Stiffening

Aortic stiffening and CAS are thought to affect coronary blood flow [1,2]. Pathological conditions such as aortic aneurysm, aortic wall stiffening and calcific aortic stenosis (CAS) will affect the distensibility of the aortic root and therefore the hemodynamics of the region. Reduced aortic distensibility (i.e. increased aortic stiffness) via presence of pathologies such as severe CAS results in a decrease of diastolic backflow. This reduction will cause less flow to enter the coronaries [2,3,4] and therefore reduce the amount of oxygen delivered to myocardium. This reduction of coronary flow can be explained by the concomitance of reduced myocardial supply as a result of decreased coronary perfusion pressure, and increased myocardial metabolic demand.

Effects of neurotensin and neuropeptide Y on coronary circulation and myocardial function in dogs

1993 ◽  
Vol 264 (4) ◽  
pp. H1062-H1068 ◽  
Author(s):  
G. Ertl ◽  
B. Bauer ◽  
H. H. Becker ◽  
G. Rose
Keyword(s):  
Myocardial Ischemia ◽  
Neuropeptide Y ◽  
Coronary Flow ◽  
Myocardial Function ◽  
Perfusion Pressure ◽  
Electromagnetic Flowmeter ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Systemic Hemodynamic ◽  
Coronary Constriction

This study analyzed the effects of the neuropeptides, neurotensin, and human and porcine analogue, neuropeptide Y, in anesthetized open-chest dogs. The left anterior descending coronary artery was cannulated and perfused at constant pressure via a blood reservoir. Flow to the coronary cannula was measured by an electromagnetic flowmeter, and regional segment lengths were measured by sonomicrometer crystals. Neurotensin injected into the coronary cannula resulted in a dose-dependent increase of coronary flow; neuropeptide Y resulted in a decrease of coronary flow. Because these changes in flow were not explained by systemic hemodynamic effects or alterations in regional myocardial function, they were considered to be coronary dilatation or constriction. Coronary dilatation by neurotensin was not prevented by alpha- or beta-adrenoceptor blockade but was completely abolished by indomethacin or by lowering coronary perfusion pressure to 35 mmHg when depressed systolic segment shortening indicated myocardial ischemia. Coronary constriction by neuropeptides Y persisted at coronary perfusion pressure of 35 mmHg and was only attenuated by indomethacin. We conclude that in contrast to systemic effects, coronary vasodilatation by neurotensin is mediated by a prostanoid product of cyclooxygenase. Preactivation of the prostaglandin system may explain why neurotensin lost its coronary dilator effect during myocardial ischemia. Neuropeptide Y may elicit coronary constriction in addition to mechanic reduction of coronary flow resembling severe coronary stenosis.

Sign in / Sign up

Export Citation Format

Share Document