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J Thorac Cardiovasc Surg 1997;114:461-466
© 1997 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

INHALED NITRIC OXIDE IS NOT A NEGATIVE INOTROPIC AGENT IN A PORCINE MODEL OF PULMONARY HYPERTENSION

Supported by the Start-Up Grant, Department of Surgery, College of Physicians and Surgeons, Columbia University.

Received for publication June 18, 1996; revisions requested Sept. 19, 1996; revisions received Feb. 13, 1997; accepted for publication Feb. 21, 1997. Address for reprints: Daniel J. Goldstein, MD, Department of Surgery, 622 West 168th St., PO Box 268, New York, NY 10032.

Abstract

Background: Reports of pulmonary edema complicating inhaled nitric oxide therapy in patients with chronic heart failure and pulmonary hypertension have raised the concern that inhaled nitric oxide may have negative inotropic effects. Methods and results: We investigated the effect of multiple doses of inhaled nitric oxide (20, 40 and 80 ppm) on left ventricular contractile state in 10 open-chest pigs. Pressure-volume loops were generated during transient preload reduction to determine the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relation. Inhaled nitric oxide had no effect on systemic vascular resistance, cardiac output, end-systolic pressure-volume relationship or stroke work-end-diastolic volume relation under normal conditions. After induction of pulmonary hypertension (intravenous thromboxane A₂ analog), inhalation of nitric oxide (80 ppm) resulted in a reduction in pulmonary vascular resistance (mean ± standard error of the mean) from 10.4 ± 3 to 6.5 ± 2 Wood units (p < 0.001) and in pulmonary artery pressure from 44 ± 4 to 33 ± 4 mm Hg (p < 0.05). Left ventricular end-diastolic volume rose from 53 ± 9 ml to 57 ± 10 ml (p = 0.02). No statistically significant change in cardiac output or systemic vascular resistance was observed. Inhaled nitric oxide had no effect on end-systolic pressure-volume relationship or stroke work-end-diastolic volume relation. Conclusions: In a porcine model of pulmonary hypertension, inhaled nitric oxide does not impair left ventricular contractile function. Therefore the cause of pulmonary edema observed in some patients receiving inhaled nitric oxide is not due to a negative inotropic action of this therapy.

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