Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs

Abstract

Cremona, George, Tim Higenbottam, Motoshi Takao, Edward A. Bower, and Leslie W. Hall. Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs. J. Appl. Physiol. 82(1): 23–31, 1997.—The site of action of endogenous and exogenous nitric oxide (NO) in isolated pig lungs was investigated by using arterial, double, and venous occlusion, which allowed precapillary, postcapillary, and venous segments to be partitioned into arterial, precapillary, postcapillary, and venous segments. N G-nitro-l-arginine (l-NNA; 10−5 M) increased resistance in the arterial (35 ± 6.6%, P = 0.003), precapillary (39.3 ± 5.1%, P = 0.001), and venous (18.3 ± 4.8%, P = 0.01) segments, respectively. Sodium nitroprusside (10−5 M) and NO (80 parts/million) reversed the effects ofl-NNA. Total pulmonary vascular resistance fell with increasing flow, due to a fall in precapillary resistance and dynamic resistance, and was significantly lower than mean total resistance.l-NNA increased the resistances but did not alter the pattern of the pressure-flow relationships. It is concluded that, in isolated pig lungs, the effect of endogenous NO seems to be dependent on flow in the arterial segment and independent of flow in the precapillary segment, but variation of its release does not appear to be fundamental to accommodation to changes in steady flow.