Autonomic cardiovascular control during hypoxia in the dog.

The mechanisms controlling cardiovascular responses to hypoxia are poorly understood. We studied effects of parasympathetdc blockade by atropine (Px) and sympathectomy by adrenalectomy plus 6-hydroxydopamine (Sx) in five unanesthetdzed dogs acutely exposed to hypoxic conditions (Paoi 35 mm Hg). In intact dogs during hypoxia, heart rate increased by 55 ± 10 (SEM) beats/min. After either Px or Sx, heart rate increased by only 34 ± 4 beats/min during hypoxia. Combined Sx and Px abolished the heart rate response to hypoxia. In intact dogs, hypoxia decreased stroke volume by 6 ± 1 ml. After Sx, hypoxia still decreased stroke volume (5 ± 1 ml), but stroke volume increased during Px (5 ± 2 ml). The stroke volume response was eliminated by Sx plus Px. Cardiac output increased during hypoxia alone (1.2 ± 0.2 liters/min) and in the presence of Px (2.0 ± 0.5 liters/min) and Sx (0.8 ± 0.3 liter/min); this response was abolished by Sx plus Px. Systemic arterial pressure increased during hypoxia alone (16 ± 4 mm Hg) and in the presence of Px (21 ± 7 mm Hg), but failed to change during either Sx or Sx plus Px. Total systemic vascular resistance fell during hypoxia alone (5 ± 2 mm Hg/ liter per min) and in the presence of Px (3 ± 1 mm Hg/liter per min and Sx (5 ± 2 mm Hg/liter per min), but failed to fall during Sx plus Px. We conclude that the autonomic nervous system plays a major role in mediating these cardiovascular systemic responses to hypoxia. The pattern of responses suggests that sympathetic activity increases heart rate, stroke volume, cardiac output, and blood pressure during hypoxia. whereas decreased parasympathetic activity increases heart rate and cardiac output and decreases stroke volume. If both components of the autonomic system are blocked, the systemic hypoxic response is eliminated. Ore Res 44: 569-676, 1979