Effect of different degrees of hypoxia and reoxygenation on myocardial energetics.
We determined the effect of high-flow hypoxia and reoxygenation on myocardial function and O2 uptake. Isolated working rat hearts were subjected to a 30-min period of hypoxia (pO2 = 384, 296, 207 and 131 torr), followed by 30 min of reoxygenation (pO2 = 500 torr). Another group of normoxic hearts was exposed to 500 torr O2 for the same length of time. During hypoxia, lactate release increased, whereas O2 uptake (VO2), aortic flow (AF) and stroke volume decreased relative to the degree of hypoxia. In hearts subjected to a pO2 of 131 torr, coronary flow and VO2 declined to 40 and 15%, respectively, of the control values, without any AF. Reoxygenation of the hypoxic hearts after the hypoxia increased the depressed VO2 and AF relative to the previous degree of hypoxia. However, these values remained below those of the normoxic hearts, indicating persistent hypoxic injury. In a second series, we also measured the mechanical power (using aortic pressure) at three levels of inflow pO2: 500, 300 and 200 torr, and obtained good correlation between the mechanical power and both AF and VO2. Analysis of the O2 cost of production of AF showed a posthypoxic disengagement between VO2 and AF after exposure to O2 of 131 torr. The degree of hypoxia determines the amount of hypoxic damage and the ability of the heart to recover upon reoxygenation, and an accelerated injury occurs at severe hypoxia.
Department of Internal Medicine C. Rambam Medical Center, Haifa, Israel.
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Edoute
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Arieli
D000818:Animals; D001011:Aorta / Q000502:physiology; D001775:Blood Circulation; D001794:Blood Pressure; D001834:Body Water / Q000378:metabolism; D002302:Cardiac Output; D003326:Coronary Circulation; D006321:Heart / Q000502:physiology; D006339:Heart Rate; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats