SITE OF PULMONARY VASODILATION BY INHALED NITRIC-OXIDE IN MICROEMBOLIC LUNG INJURY

We investigated the site of pulmonary vasodilation and associated effe cts on gas exchange in response to inhaled NO in acute microembolic lu ng injury. Pulmonary arterial (Ppa) and effective capillary (Pc') pres sures versus cardiac output ((Q) over dot) plots were generated in ane sthetized dogs before and after, successively, (1) embolization with 1 00 mu m glass beads, (2) administration of either a placebo (n = 5) or 80 ppm inhaled NO followed by cyclooxygenase inhibition by aspirin 1 g given intravenously and again 80 ppm inhaled NO (n = 8), Pc' was est imated from the pressure decay curve after pulmonary artery balloon oc clusion. Embolism increased pulmonary vascular resistance, with a slig ht decrease in its precapillary component, from 77 to 66%. NO decrease d Ppa at the highest levels of (Q) over dot, and aspirin increased Ppa at all levels of (Q) over dot. Neither NO nor aspirin affected Pc'/(Q ) over dot plots or pulmonary shunt. We conclude that pulmonary vascul ar resistance in microembolic lung injury increases at the periphery o f the pulmonary arterial tree, with partial reversibility by inhaled N O and by endogenous products of the cyclooxygenase pathway upstream fr om the site of effective capillary resistance. Reduced pulmonary vascu lar tone does not improve gas exchange in this model of acute lung inj ury.