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We have studied the interrelations of myocardial oxygen metabolism and myocardial blood flow in hemorrhagic shock. Myocardial blood flow was measured by the 133Xe-washout method in closed-chest anesthetized dogs while the dogs were breathing either room air at ambient pressure or oxygen at high pressure. In animals with normal blood pressure, oxygen at high pressure produced a consistent decrease in myocardial blood flow from a mean of 70 ml/100 g/min to a mean of 43 ml/100 g/min, with a proportionate decrease in myocardial O2 consumption. In animals in hemorrhagic shock, oxygen at high pressure induced no change in myocardial blood flow but increased myocardial O2 consumption from a mean of 5.9 ml/100 g/min to a mean of 7.4 ml/100 g/min. When the animals in hemorrhagic shock breathed room air again at ambient pressure following oxygen at high pressure, the myocardial blood flow increased from a mean of 40 ml/100 g/min to a mean of 51 ml/100 g/min. The myocardial O2 consumption did not change. We conclude that with decreasing blood pressure a baseline of myocardial blood flow may be reached, so that a further decrease no longer occurs in response to hyperoxia. However, the control of myocardial blood flow in shock is an active process responsive to complex positive control mechanisms that may be altered and studied experimentally.

Myocardial Oxygen Metabolism and Myocardial Blood Flow in Dogs in Hemorrhagic Shock