Abstract

In this study of the efficacy of hyperbaric oxygenation in the therapy of left ventricular failure after experimental myocardial infarction, 6 intact dogs underwent a 20 minute control period of exposure to 100 percent oxygen at 3 atmospheres absolute of pressure. The procedure increased arterial PO 2 to more than 1,600 mm Hg and mean aortic pressure by 8 percent (0.05 < P < 0.10); left ventricular end-diastolic pressure increased from 8.0 to 9.7 mm Hg ( P < 0.05) without change in heart rate, cardiac output, stroke volume, left ventricular minute work, stroke work or total peripheral resistance. One hour later, coronary occlusion was produced and resulted in left ventricular failure, manifested by an increase in heart rate and left ventricular end-diastolic pressure and by a fall in stroke volume and stroke work. Ten minutes after occlusion, the dogs underwent a second hyperbaric exposure period, and mean aortic pressure increased by 9 percent (0.05 < P < 0.10), left ventricular minute work by 9 percent ( P < 0.01) and stroke work by 17 percent (0.05 < P < 0.10). The increased work was performed at the expense of an increase in left ventricular end-diastolic pressure from 13.1 to 17.4 mm Hg ( P < 0.01). Other variables remained stable. An additional 8 dogs that underwent coronary occlusion while breathing room air had stable hemodynamic values over the ensuing hour except for a progressive increase in left ventricular end-diastolic pressure. It is concluded that hyperbaric oxygenation did not improve left ventricular function impaired by experimental myocardial infarction in intact, conscious dogs, even though given at a time when the ischemic lesion was potentially reversible.

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