AJP - Regulatory, Integrative and Comparative Physiology, Vol 245, Issue 2 143-R150, Copyright © 1983 by American Physiological Society
Cardiovascular functions during voluntary apnea in dogs
Y. C. Lin, E. L. Carlson, E. P. McCutcheon and H. Sandler
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.
