triolein and Respiratory-Distress-Syndrome

Pathophysiologic mechanisms of the fat embolism syndrome are poorly understood. Neutrophils are thought to play a role in the development of many forms of acute lung injury. The objective of this study was to examine the role of intrapulmonary neutrophils in lung injury resulting from fat infusion.. Triolein (0.08 mL/kg) was infused into isolated rabbit lungs perfused with Krebs-Henseleit buffer. Pulmonary arterial pressure was monitored, and pulmonary vascular resistance and microvascular permeability (Kf) were measured at baseline and 60 minutes after triolein infusion.. Triolein produced increases in pulmonary arterial pressure, pulmonary vascular resistance, and Kf. Neutrophil depletion or inhibition of neutrophil elastase prevented the increase in Kf after triolein, and catalase partially blocked this Kf increase.. These results suggest that activated intrapulmonary neutrophils play a major role in developing triolein-induced lung injury, intrapulmonary neutrophils act chiefly via neutrophil elastase release, and reactive oxygen species are involved in the lung injury.

Topics: Animals; Blood Pressure; Capillary Permeability; Disease Models, Animal; Embolism, Fat; Hemodynamics; Lung; Microcirculation; Neutrophils; Peroxidase; Rabbits; Respiratory Distress Syndrome; Triolein; Vascular Resistance

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.. 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.. 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.. 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.

Topics: 1-Methyl-3-isobutylxanthine; Animals; Blood Pressure; Capillary Permeability; Cyclooxygenase Inhibitors; Dose-Response Relationship, Drug; Embolism, Fat; In Vitro Techniques; Indomethacin; Lung; Male; Microcirculation; Muscle, Smooth, Vascular; Phosphodiesterase Inhibitors; Pulmonary Artery; Pulmonary Circulation; Pulmonary Embolism; Rats; Rats, Wistar; Respiratory Distress Syndrome; Triolein; Vascular Resistance

Topics: Animals; Dogs; Embolism, Fat; Lung; Respiratory Distress Syndrome; Triolein