An Analysis of Postvagal Inotropic Responses

Stimulation of the right cervical vagosympathetic trunk in the chloralose-anesthetized, decentralized dog was followed by a two-component postvagal inotropic response: an initial return of contractility toward the control level, but significantly less than control and a secondary, more delayed, significant positive inotropic effect compared to control contractility. Maintenance of arterial pressure by ventricular pacing during vagal stimulation eliminated the late positive inotropic effect but not the early response. Occlusion of the inferior vena cava for 15-20 sec immediately following vagal stimulation delayed the late positive inotropic effect for a period equal to the duration of the occlusion. Blockade of muscarinic cholinergic receptors (atropine) eliminated the late response as did blockade of beta adrenergic receptors (propranolol). Block of catecholamine release from sympathetic endings (guanethidine) had no effect on the late response. It is concluded that adrenal medullary catecholamines, released presumably as a consequence of vagally-induced hypotension, are responsible for the late positive inotropic effect produced following vagal stimulation.