The Sympathoadrenergic System in the Cardiovascular Responses to Hypoxia in the Dog

Abstract

The role of the sympathoadrenergic system in the cardiovascular responses during the steady state of acute severe hypoxia (6% O2 in N2 for 15 min) was studied in 49 anesthetized dogs divided into five groups: sham-operated, sympathectomized (stellate to T5), intact untreated, and pronethalol-treated (2.5 and 5.0 mg/kg i.v.). In a separate group of animals, the steady state as to O2 consumption, arterial and venous O2 saturation, blood respiratory quotient, and ventilation was investigated and found to be present between 10–15 min after the onset of acute hypoxia. Under these experimental conditions cardiac output rose significantly in the sham-operated, sympathectomized, and intact groups. This increase occurred on the basis of tachycardia in the intact untreated group and a combination of increased heart rate and stroke volume in the operated groups. In contrast, beta adrenergic blockade with pronethalol prevented the rise in cardiac output through a combination of reduced tachycardia and a fall in stroke volume at the end of the 15 min of hypoxia. It is concluded that during the steady state of acute hypoxia, stimulation of cardiac beta adrenergic receptors by a humoral mechanism plays an important role in the cardiovascular responses observed in anesthetized dogs, and that the cardiac sympathetic nerves are not essential for these responses to occur.