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

Background: Reports of pulmonary edema complicating inhaled nitric oxi de therapy in patients with chronic heart failure and pulmonary hypert ension have raised the concern that inhaled nitric oxide may have nega tive inotropic effects, Methods and results: We investigated the effec t of multiple doses of inhaled nitric oxide (20, 40 and 80 ppm) on lef t ventricular contractile state in 10 open-chest pigs, Pressure-volume loops were generated during transient preload I eduction to determine the end-systolic pressure-volume relationship and the stroke work-end -diastolic volume relation, Inhaled nitric oxide had no effect on syst emic vascular resistance, cardiac output, end-systolic pressure-volume relationship or stroke work-end-diastolic volume relation under norma l conditions, After induction of pulmonary hypertension (intravenous t hromboxane A(2) analog), inhalation of nitric oxide (80 ppm) resulted in a reduction in pulmonary vascular resistance (mean +/- standard err or of the mean) from 10.4 +/- 3 to 6.5 +/- 2 Wood units (p < 0.001) an d in pulmonary artery pressure from 44 +/- 4 to 33 +/- 4 mm Hg (p < 0. 05). Left ventricular end-diastolic volume rose from 53 +/- 9 mi to 57 +/- 10 mi (p = 0.02), No statistically significant change in cardiac output or systemic vascular resistance was observed, Inhaled nitric ox ide had no effect on end-systolic pressure-volume relationship or stro ke 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 ede ma observed in some patients receiving inhaled nitric oxide is not due to a negative inotropic action of this therapy.