Citation

McCormack DG. New Horiz. 1995; 3(2): 248-256.

Affiliation

A. C. Burton Vascular Biology Laboratory, Victoria Hospital, London, ON, Canada.

Copyright

(Copyright © 1995, Williams and Wilkins and the Society)

DOI

unavailable

PMID

7583166

Abstract

The two commonly recognized sequelae of acute lung injury (ALI) are pulmonary hypertension and arterial hypoxemia. The mechanism of the pulmonary hypertension is not precisely known, but undoubtedly is contributed to by both vasoactive mediators and pulmonary parenchymal structural changes. The pulmonary circulation is normally tightly controlled such that there is excellent matching of perfusion to ventilation through attenuation of hypoxic pulmonary vasoconstriction (HPV). In ALI, there is an attenuation of HPV and resulting areas of low ventilation/perfusion or shunt. The mechanism behind this abnormal pulmonary vascular contractility in disease is under investigation, but may involve the release of endogenous vasodilator mediators such as nitric oxide.

Language: en