The Cardiovascular Action of Oxygen Breathing: Effect on Adrenergic Stimulation

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Abstract
Anesthetized mechanically ventilated dogs (20) received an infusion of epinephrine, 2 .mu.g/kg per min, for 4 h. Dogs (10) were ventilated with air for the entire 4-h period and 10 were ventilated with O2 for the 1st h and then air for 3 h. During the 1st h of the epinephrine infusion in the group ventilated with O2, as compared to the group ventilated with air, the heart rate decreased (it increased in the dogs ventilated with air); the cardiac output increased less; the systemic vascular resistance decreased less; the pulmonary vascular resistance decreased more; and the pulmonary artery wedge pressure increased (it decreased in the dogs ventilated with air). During the next 3 h when the animals were ventilated with air, the effects of O2 on the hemodynamic changes induced by epinephrine persisted for variable periods. The epinephrine-induced pulmonary arteriovenous shunt was significantly less at all times in the group ventilated with O2, not only during the O2 breathing but following it for 3 h. O2 breathing has been known to exert powerful effects on the heart, and the pulmonary and systemic circulations in normal man and animals and in patients with pulmonary hypertension and acute respiratory failure. O2 breathing apparently significantly alters the cardiovascular effects of epinephrine during O2 breathing and reduces the epinephrine-induced pulmonary shunt during and for several hours after O2 is discontinued. Hyperoxia apparently affects, by unknown mechanisms, the autonomic regulation of the cardiovascular system.