Role of nitric oxide in vasoreactivity caused by experimental pulmonary microembolism

Abstract

Pulmonary hypertension caused by acute pulmonary embolism has been attributed to mechanical obstruction of the pulmonary arteries and also to vasoconstriction. We examined the role of nitric oxide in the vasoreactivity associated with pulmonary microembolism. Two kinds of microemboli of similar size were used: thorny microemboli (lycopodium spores, LP) and smooth microemboli (latex microspheres, MS). In isolated rat lungs perfused with blood, five injections of LP or MS into the pulmonary artery each caused a rapid increase in mean perfusion pressure, followed by a slow fall to a new, higher base line. Vasoconstriction was significantly greater after embolization with LP than after embolization with MS. Preadministration of L-NMMA, a nitric oxide synthase inhibitor, enhanced the increase in mean perfusion pressure caused by embolization with LP, but not the increase caused by embolization with MS. Before embolization, acetylcholine caused slight vasodilation. After embolization with MS, acetylcholine caused vasodilation; but after embolization with LP, acethlcholine caused vasoconstriction. Thus, we conclude that repeated embolization with LP may cause endothelial injury, and that nitric oxide may protect against pulmonary hypertension induced by LP emboli.