In the conscious, intact, instrumented dog exposure to 6 min of arterial hypoxia (Pao 24.5 mm Hg) by a mask caused a 79% increase in cardiac output, a 61% rise in heart rate, and a 22% rise in blood pressure. Ventilation increased 323%, causing hypocapnia and an increase in arterial pH. The carotid and aortic depressor nerves were then sectioned, and after a several day recovery period the effect of hypoxia was again tested. After denervation, similar levels of arterial hypoxia caused a 64% rise in cardiac output, a 23% rise in heart rate, and no change in blood pressure. There was a slight but significant increase in ventilation (20%) along with no appreciable changes in arterial pH or PCO 2. These data indicate that blood pressure is relatively well maintained during hypoxia in the awake dog after chemodenervation in contrast to the marked fall in blood pressure observed under these conditions in anesthetized dogs. Moreover, it is apparent that a large part of the cardiac output response of the intact animal is initiated outside the sinoaortic zones.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of applied physiology|
|State||Published - Dec 1 1973|
ASJC Scopus subject areas
- Physiology (medical)