Reflex effects of cephalic hypoxia, hypercapnia, and ischemia upon ventricular contractility.

Abstract

The effects of brief periods of cephalic hypoxia, hypercapnia, and ischemia upon the contractility of the normally oxygenated ventricular myocardium were studied in an innervated, isovolumetric, canine left ventricle preparation. The majority of responses to cephalic hypoxia were of two types in preparations with vagi and carotid sinus nerves still intact. (a) More frequently, peak left ventricular pressure changed in biphasic fashion, consisting of an initial depression of contractility followed by subsequent augmentation. (b) Less frequently, a monophasic enhancement of contractility appeared. After transection of either the vagi or the carotid sinus nerves, a monophasic facilitation of contractility was usually evoked by cephalic hypoxia. From these data, it was concluded that two opposing influences act simultaneously upon the ventricular myocardium during cephalic hypoxia in preparations with intact vagi and carotid sinus nerves. Central nervous system hypoxia enhances myocardial contractility; its effect is mediated principally via sympathetic pathways. Hypoxia at the level of the carotid chemoreceptors depresses contractility reflexly; the efferent limb of this reflex is mediated chiefly via the vagi. At any moment in time, the effect upon ventricular contractility is the result of these opposing influences. Cephalic hypercapnia produced effects similar to those of hypoxia. Cephalic ischemia always evoked a marked, positive inotropic effect upon the ventricles.