Attenuation of Hypoxic Pulmonary Vasoconstriction in Acute Oleic Acid Lung Injury — Significance of Vasodilator Prostanoids

Abstract

In order to assess the physiological abnormalities and the pathogenesis of adult respiratory distress syndrome (ARDS), especially that associated with pulmonary fat embolism, acute lung injury caused by monounsaturated nonsterified fat oleic acid (cis-9-octadecenoic acid) has been widely used in animal experiments. This lung injury results in an extensive, multifocal, and heterogeneously distributed lung damage with alveolar flooding, interstitial edema and microatelectasis. These morphological changes have generally been considered to develop significant shunt flow causing severe hypoxemia and loss of lung compliance. Based on the microscopic examinations, however, Schoene et al. (1984) have failed to demonstrate a quantitative relationship between the morphological alterations and the amount of shunt in dogs with lung damage induced by oleic acid administration. Further, Brigham et al. (1983) have shown that gas exchange abnormality in patients with ARDS does not correlate with extent of pulmonary edema estimated from extravascular lung water but significantly with vascular permeability-surface area. They have inferred from their experimental findings that the ability of the lung circulation to reduce perfusion of damaged and edematous areas is essentially important in preserving blood oxygenation in ARDS.