No evidence for blood flow redistribution with isoflurane or halothane during acute coronary artery occlusion in fentanyl-anesthetized dogs

The present study examines the postulate that isoflurane, in contrast to halothane, causes redistribution of blood flow away from an ischemic myocardial region through vasodilation of adjacent normally perfused myocardium. The study was performed in open-chest dogs anesthetized with fentanyl; ischem...

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Bibliographic Details
Published in:Anesthesiology (Philadelphia) 1991-11, Vol.75 (5), p.854-865
Main Authors: MOORE, P. G, KIEN, N. D, REITAN, J. A, WHITE, D. A, SAFWAT, A. M
Format: Article
Language:English
Subjects:
Anesthetics. Neuromuscular blocking agents
Animals
Biological and medical sciences
Coronary Disease - metabolism
Coronary Vessels - drug effects
Dogs
Female
Fentanyl
Halothane - pharmacology
Hemodynamics - drug effects
Isoflurane - pharmacology
Lactates - blood
Male
Medical sciences
Neuropharmacology
Oxygen Consumption
Pharmacology. Drug treatments
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Summary:The present study examines the postulate that isoflurane, in contrast to halothane, causes redistribution of blood flow away from an ischemic myocardial region through vasodilation of adjacent normally perfused myocardium. The study was performed in open-chest dogs anesthetized with fentanyl; ischemia was induced by occlusion of the left anterior descending coronary artery. At 0.6% alveolar concentration, isoflurane increased transmural blood flow to 125% of control values (P less than 0.05) in the normal region without concomitant changes in blood flow to the ischemic region or in the endocardial/epicardial flow ratio in the ischemic region. The evidence excludes either transmural steal or regional redistribution phenomena. Myocardial blood flow variables returned to control values at 1.8% isoflurane, and no blood flow redistribution effects were evident. In contrast, whereas halothane 0.4% caused no significant effect on myocardial blood flows, an alveolar concentration of 1.2% decreased transmural blood flow to normally perfused left ventricle to 70% of control (P less than 0.05). Regional myocardial oxygen consumption in the normal and ischemic areas decreased at higher alveolar concentrations and was unchanged at the lower concentrations for both agents. Myocardial lactate production from the ischemic region was unchanged with either agent, suggesting that, in terms of metabolic changes, neither agent worsened ischemia during sustained occlusion of the left anterior descending coronary artery. The present data show no evidence for worsening of myocardial ischemia with either isoflurane or halothane. Isoflurane causes a relatively greater increase in perfusion compared to myocardial oxygen consumption of normally perfused myocardium; nevertheless, sufficient coronary vascular reserve remains in the native collateral circulation so that myocardial metabolic supply-and-demand relationships during ischemia are not further compromised.
ISSN:0003-3022
1528-1175
DOI:10.1097/00000542-199111000-00018