LACK OF EFFECT OF INHALED NITRIC-OXIDE IN SYSTEMIC AND PULMONARY-HYPERTENSION DUE TO ACUTE SINE-AORTIC DENERVATION

Inhaled nitric oxide, a selective pulmonary vasodilator, reverses hypo xic pulmonary vasoconstriction and is an effective treatment in some c ases of human pulmonary hypertension. Localization of nitric oxide syn thase had indicated a neural role for nitric oxide. Thus, we studied t he interactions between inhaled nitric oxide and systemic and pulmonar y vascular reactivity in acute neurogenic hypertension. In 6 male beag le dogs (mean weight: 15 +/- 1 kg), anesthetized by chloralose (8 cg/k g) and in spontaneous ventilation, the hemodynamic effects on systemic and pulmonary circulation of inhaled nitric oxide (12 ppm) were studi ed before and after acute sine-aortic denervation. The hemodynamic eff ects of intravenous propranolol (300 mu g/kg) were studied after dener vation. Mean arterial pressure (MAP), pulmonary capillary pressure (PC P), mean arterial pulmonary pressure (MAPP), cardiac imput (CI) and ox ygene venous saturation (SvO(2)) were measured. GRAPHICS Sino-aortic denervation causes an acute and transitory pulmonary hypertension due to a double mechanism: a post-capillary hypertension (increase PCP) s econdary to an increase left ventricular post-charge by systemic hyper tension and a precapillary hypertension. In fact, vascular pulmonary r esistances increase from 1.8 +/- 0.1 to 3.4 +/- 0.8 uW after denervati on (p < 0.05). Change in pulmonary vascular reactivity induced by cate cholamines is probably involved. Propranolol but not inhaled nitric ox ide reverses pulmonary hypertension due to sine-aortic denervation.