Autonomic cardiovascular control during hypoxia in the dog.

Abstract

The mechanisms controlling cardiovascular responses to hypoxia are poorly understood. Atropine parasympathetic blockade (Px) and sympathectomy by adrenalectomy plus 6-hydroxydopamine (Sx) was studied in 5 unanesthetized dogs exposed to hypoxic conditions (O2 arterial partial pressure, PaO2 = 35 mm Hg). In intact dogs during hypoxia, heart rate increased by 55 .+-. 10 (SEM [standard error of the mean]) 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 l/min) and in the presence of Px (2.0 .+-. 0.5 l/min) and Sx (0.8 .+-. 0.3 l/min); the response was abolished by Sx plus Px. Systemic arterial pressure increased during hypoxia alone (16 .+-. 4 mm Hg) qnd in the presence of Px (21 .+-. 7 mm Hg), but failed to change during Sx or Sx plus Px. Total systemic vascular resistance fell during hypoxia alone (5 .+-. 2 mm Hg/l per min) and in the presence of Px (3 .+-. 1 mm Hg/l per min) and Sx (5 .+-. 2 mm Hg/l per min), but failed to fall during Sx plus Px. Apparently the autonomic nervous system plays a major role in mediating 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.