Background: The pathophysiologic mechanism of the fat embolism syndrome is poorly understood. This study was designed to determine the effects of fat emboli on pulmonary vasculature.
Method: Triolein was infused into isolated rat lungs perfused with Krebs-Henseleit buffer. Pulmonary arterial pressure and microvascular permeability (Kf) were measured at baseline and 20 minutes after the triolein infusion.
Result: The 99% triolein produced dose-dependent increases in both pulmonary arterial pressure and Kf. The 65% triolein, containing free fatty acid, resulted in a greater increase in Kf. Pretreatment with indomethacin attenuated the increase in Kf after 65% triolein but not after 99% triolein.
Conclusion: Pure triolein induced mainly embolization in the pulmonary vasculature, and 65% triolein caused embolization and subsequently increased vascular permeability, which are, at least in part, mediated by the action of cyclooxygenase products. Free fatty acids might induce permeability edema by means of a cyclooxygenase-dependent mechanism. We conclude that triolein-induced increases in pulmonary arterial pressure and Kf in isolated rat lungs provides a useful model of acute lung injury by fat embolism.