| Abstract: | ![]()
20 anesthetized mechanically ventilated dogs received an infusion of epinephrine, 2 micrograms/kg/min, for 4 h. 10 dogs were ventilated with air for the entire 4-hour period and 10 were ventilated with oxygen for the first hour and then air for 3 h. During the first hour of the epinephrine infusion in the group ventilated with oxygen, 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 oxygen 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 oxygen, not only during the oxygen breathing but following it for 3 h. Oxygen 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. This study demonstrates that oxygen breathing significantly alters the cardiovascular effects of epinephrine during oxygen breathing and reduces the epinephrine-induced pulmonary shunt during and for several hours after oxygen is discontinued. These finding add further evidence that hyperoxia affects, by unknown mechanisms, the autonomic regulation of the cardiovascular system. |
