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J Thorac Cardiovasc Surg 1998;115:700-704
© 1998 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

Inhaled Nitric Oxide Is Not A Myocardial Depressant In A Porcine Model Of Heart Failure

From the Divisions of Cardiothoracic Surgery^a and Circulatory Physiology^b and the Department of Anesthesiology,^c Columbia University College of Physicians and Surgeons, New York, N.Y.

Received for publication April 22, 1997; revisions requested July 29, 1997; revisions received Oct. 16, 1997; accepted for publication Oct. 16, 1997. Address for reprints: Michael Argenziano, MD, Division of Cardiothoracic Surgery, Milstein Hospital Building, Room 7-435, 177 Fort Washington Ave., New York, NY 10032.

Abstract

Background: Inhaled nitric oxide has been shown to be a potent and selective pulmonary vasodilator. Reports of increases in left ventricular end-diastolic pressure and episodes of pulmonary edema during the clinical use of inhaled nitric oxide in patients with preexisting left ventricular dysfunction have raised concerns that this agent may have myocardial depressant effects. We therefore undertook a study of the effects of inhaled nitric oxide on myocardial contractility in a porcine model of ventricular failure and pulmonary hypertension.
Methods: After inducing heart failure in 10 pigs by rapid ventricular pacing, hemodynamic measurements and pressure-volume diagrams (by the conductance method) were obtained in six animals at baseline and during administration of inhaled nitric oxide at concentrations of 20 and 40 ppm. Myocardial contractile state was assessed by the end-systolic pressure-volume relationship and preload-recruitable stroke work, whereas diastolic function was measured in terms of the end-diastolic pressure-volume relationship and the pressure decay time constant T.
Results: Baseline hemodynamics reflected heart failure and pulmonary hypertension, and inhaled nitric oxide induced significant reductions in mean pulmonary artery pressure and pulmonary vascular resistance. Although left ventricular end-diastolic pressure increased during administration of inhaled nitric oxide, no changes were observed in measures of systolic or diastolic function.
Conclusions: Inhaled nitric oxide reduced pulmonary vascular resistance but did not alter myocardial contractility or diastolic function. Increases in left ventricular end-diastolic pressure during inhaled nitric oxide therapy are therefore not due to myocardial depression and may be related to increases in volume delivery to the left side of the heart resulting from reduced pulmonary vascular resistance.

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