Depression of Ventricular Contractility by Stimulation of the Vagus Nerves

In three different types of canine heart preparations, it was demonstrated that efferent vagal stimulation exerts a potent, negative inotropic influence upon the ventricular myocardium. In the paced, isovolumetric, left ventricle preparation, vagal stimulation evoked a reduction of left ventricular systolic pressure which, within limits, varied directly with the magnitude of the stimulus. Supramaximal stimulation elicited a mean reduction of 23% in the peak pressure generated by the left ventricle. No differences could be detected between the effects of the right and left vagi upon ventricular contractility. The percentage changes induced by vagal stimulation upon ventricular contractility in the paced heart were less than the percentage changes in heart rate induced in the spontaneously beating heart. In a pumping heart preparation in which a constant rate of venous return was delivered to the left atrium, vagal stimulation consistently elicited an appreciable elevation of left ventricular end diastolic pressure. Another pumping heart preparation was employed in which changes in atrial transport function and mitral valve closure were excluded by the expedient of introducing a balloon into the left ventricle through an apical incision. This balloon was connected to an artificial external circuit with fixed venous reservoir height and peripheral resistance. Vagal stimulation consistently diminished stroke volume, "arterial" pressure, and stroke work in such a circuit.