Cardiovascular functions during voluntary apnea in dogs.

We studied cardiovascular responses to apnea during voluntary snout immersion in conscious, chronically instrumented dogs. Voluntary snout immersion up to eye level for a duration of greater than 15 s ensured that the dog was engaged in active apnea. In a control apnea of 15-35 s, heart rate decreased by 43% from a control value of 104 beats/min. Changes in cardiac output paralleled those of heart rate. Mean aortic blood pressure did not vary during apnea, which, coupled with a reduced cardiac output, indicated a 65% increase in estimated total peripheral resistance compared with preapnea values. Treatment with atropine sulfate (0.2 mg/kg) eliminated the bradycardia response, but the peripheral vasoconstriction persisted. Treatment with propranolol (0.5 mg/kg) eliminated postapnea hypertension. Changes in myocardial contractility during apnea were observed by measuring hemodynamic parameters while maintaining a constant heart rate with cardiac pacing. Myocardial contractility was decreased during apnea as indicated by decreases in stroke volume (-13%), stroke work (-22%), cardiac output (-13%), left ventricular (dP/dt)max (-11%), and cardiac power (-24%). These changes were prevented by atropine treatment, indicating the depressed contractility was a result of vagus nerve activity. The circulatory adjustments in the dog during apnea are potential mechanisms for oxygen conservation, although the effectiveness is uncertain for the animal as a whole. It is clear that by appropriate reduction in cardiac power output, the heart itself plays an active role in conservation of limited oxygen during apnea.