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Am. J. Respir. Crit. Care Med., Volume 156, Number 1, July 1997, 75-85

Site of Pulmonary Vasodilation by Inhaled Nitric Oxide in Microembolic Lung Injury

CHRISTIAN MÉLOT, FRANÇOISE VERMEULEN, MARCO MAGGIORINI, ERIC GILBERT, and ROBERT NAEIJE

The Laboratory of Cardiovascular and Respiratory Physiology, Erasme University Hospital, Brussels, Belgium

We investigated the site of pulmonary vasodilation and associated effects on gas exchange in response to inhaled NO in acute microembolic lung injury. Pulmonary arterial (Ppa) and effective capillary (Pc') pressures versus cardiac output (Q) plots were generated in anesthetized dogs before and after, successively, ( 1) embolization with 100 µm 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 estimated from the pressure decay curve after pulmonary artery balloon occlusion. Embolism increased pulmonary vascular resistance, with a slight decrease in its precapillary component, from 77 to 66%. NO decreased Ppa at the highest levels of Q, and aspirin increased Ppa at all levels of Q. Neither NO nor aspirin affected Pc '/Q plots or pulmonary shunt. We conclude that pulmonary vascular resistance in microembolic lung injury increases at the periphery of the pulmonary arterial tree, with partial reversibility by inhaled NO and by endogenous products of the cyclooxygenase pathway upstream from the site of effective capillary resistance. Reduced pulmonary vascular tone does not improve gas exchange in this model of acute lung injury.




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