Abstract

Acute pulmonary vasoconstriction occurs in a variety of clinical settings relevant for the cardiac intensivist, postoperative pulmonary hypertension being perhaps the most common. Although we know that significant postoperative pulmonary vasoconstriction generally occurs in patients with a pathologically remodeled pulmonary circulation, we know little of its pathophysiology. The following review describes the biochemistry of smooth muscle contractile activation and examines the possible role that endothelin-1 may play in postoperative pulmonary hypertension.

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