LOCAL AND NEURALLY MEDIATED EFFECTS OF MORPHINE ON SKELETAL MUSCLE VASCULAR RESISTANCE

¹ Anaesthesia Laboratory of the Harvard Medical School at the Massachusetts General Hospital, the Cardiac Unit of the Massachusetts General Hospital and the Departments of Anaesthesia and Medicine, Harvard Medical School, Boston, Massachusetts

Morphine caused both a local and a neurally mediated decrease in skeletal muscle vascular resistance of the isolated canine gracilis muscle preparation which was separately perfused with blood at a near constant flow. The local (gracilis artery injection, acutely denervated muscle) decrease was consistent, dose-dependent and reversible with time. An initial, transient neurally mediated (systemic i.v. injection, innervated muscle) decrease in vascular resistance was present if control resistance was higher than denervated resistance. This decrease appeared secondary to central sympatholysis or ganglionic sympathetic blockade, since it was unaffected by cholinergic blockade, cervical vagotomy or carotid sinus denervation but was absent if control resistance approximated denervated vascular resistance or if the muscle had received a previous alpha adrenergic receptor blockade. A sustained elevation of muscle vascular resistance of the innervated muscle occurred regardless of whether or not the initial neurally mediated decrease was present. Presumably this represented a reflex compensation for the direct local vasodilatory effect of morphine. These data suggest central withdrawal of vasomotor tone as a mechanism for the hypotension after morphine administration and may explain the variable peripheral circulatory response to morphine observed clinically.