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.

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

Alteration in myocardial oxygen balance during exercise after beta-adrenergic blockade in dogs

1980 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
G. R. Heyndrickx ◽  
J. L. Pannier ◽  
P. Muylaert ◽  
C. Mabilde ◽  
I. Leusen
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Oxygen Balance

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.

Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline

1989 ◽  
Vol 257 (4) ◽  
pp. H1043-H1048 ◽  
Author(s):  
H. M. Wei ◽  
Y. H. Kang ◽  
G. F. Merrill
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Vasodepressor Response

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.

Alpha 1-adrenergic constriction limits coronary flow and cardiac function in running dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1117-H1126 ◽  
Author(s):  
P. A. Gwirtz ◽  
S. P. Overn ◽  
H. J. Mass ◽  
C. E. Jones
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Receptor Blocker ◽  
Adrenergic Blockade

Modulation of coronary blood flow and cardiac function by alpha 1-adrenergic receptors was examined in dogs during strenuous exercise. Fifteen dogs were chronically instrumented to measure left circumflex blood flow, heart rate, regional left ventricular function (systolic shortening, and rate of shortening), and global left ventricular function (left ventricular pressure, and dP/dt). The specific postsynaptic alpha 1-receptor blocker prazosin (0.5 mg) and nonselective alpha-receptor blocker phentolamine (1.0 mg) were injected through an indwelling circumflex artery catheter to produce local adrenergic blockade of the posterior left ventricular region during exercise. Exercise significantly increased heart rate, left ventricular systolic pressure, dP/dt, segment shortening and rate of shortening, and coronary blood flow. Both prazosin and phentolamine caused similar additional increases in dP/dt by 21 +/- 4%, in rate of shortening in the posterior region by 37 +/- 6%, and in myocardial O2 consumption by 26 +/- 11%, which were associated with a 21 +/- 3% increase in coronary flow during exercise but no change in O2 extraction. Similar results were obtained when dogs were beta-blocked with either atenolol (1.0 mg ic) or propranolol (1.0 mg ic) prior to exercise. These data suggest that an alpha 1-vasoconstriction modulates O2 delivery to myocardial tissue and limits both coronary vasodilation and cardiac function during exercise.

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.

Influence of low perfusion pressure on effect of endothelin on coronary vascular bed

1991 ◽  
Vol 260 (3) ◽  
pp. H893-H901 ◽  
Author(s):  
J. P. Clozel ◽  
U. Sprecher
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Perfusion Pressure ◽  
Coronary Spasm ◽  
Electromagnetic Flowmeter ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Cross Sectional ◽  
Coronary Vasoconstriction

The goal of this study was to evaluate the influence of low coronary perfusion pressure on the coronary vasoconstriction induced by endothelin. For this purpose, the circumflex coronary arteries of 12 open-chest dogs were cannulated and perfused at a controlled pressure. Total coronary blood flow was measured with an electromagnetic flowmeter and the transmural distribution of coronary blood flow with the radioactive microspheres technique. In addition, the circumflex coronary artery diameter was measured by sonomicrometry with piezoelectric crystals, and the coronary cross-sectional area was calculated. At a coronary perfusion pressure of 100 mmHg, endothelin induced a marked coronary vasoconstriction and a redistribution of coronary blood flow toward the endocardium. At a low coronary perfusion pressure of 40 mmHg, these effects of endothelin were still present. The constriction of the large coronary artery occurred even with a lower dose of endothelin at a low coronary perfusion pressure compared with the normal perfusion pressure. This was not the case when angiotensin II was given the same way. We conclude that endothelin is a potent coronary vasoconstrictor even at a low perfusion pressure. Thus one may speculate that endothelin plays a role in the coronary spasm which has been shown in patients with angina pectoris.

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.

Standard CPR versus interposed abdominal compression CPR in shunted single ventricle patients: comparison using a lumped parameter mathematical model

2021 ◽  
pp. 1-7
Author(s):  
Daniel Stromberg ◽  
Karen Carvalho ◽  
Alison Marsden ◽  
Carlos M. Mery ◽  
Camille Immanuel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Pulmonary Blood Flow ◽  
Single Ventricle ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Lumped Parameter

Abstract Introduction: Cardiopulmonary resuscitation (CPR) in the shunted single-ventricle population is associated with poor outcomes. Interposed abdominal compression-cardiopulmonary resuscitation, or IAC-CPR, is an adjunct to standard CPR in which pressure is applied to the abdomen during the recoil phase of chest compressions. Methods: A lumped parameter model that represents heart chambers and blood vessels as resistors and capacitors was used to simulate blood flow in both Blalock-Taussig-Thomas and Sano circulations. For standard CPR, a prescribed external pressure waveform was applied to the heart chambers and great vessels to simulate chest compressions. IAC-CPR was modelled by adding phasic compression pressure to the abdominal aorta. Differential equations for the model were solved by a Runge-Kutta method. Results: In the Blalock-Taussig-Thomas model, mean pulmonary blood flow during IAC-CPR was 30% higher than during standard CPR; cardiac output increased 21%, diastolic blood pressure 16%, systolic blood pressure 8%, coronary perfusion pressure 17%, and coronary blood flow 17%. In the Sano model, pulmonary blood flow during IAC-CPR increased 150%, whereas cardiac output was improved by 13%, diastolic blood pressure 18%, systolic blood pressure 8%, coronary perfusion pressure 15%, and coronary blood flow 14%. Conclusions: In this model, IAC-CPR confers significant advantage over standard CPR with respect to pulmonary blood flow, cardiac output, blood pressure, coronary perfusion pressure, and coronary blood flow. These results support the notion that single-ventricle paediatric patients may benefit from adjunctive resuscitation techniques, and underscores the need for an in-vivo trial of IAC-CPR in children.

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