The Pathophysiology of Smoke Inhalation Injury in a Sheep Model

Abstract

An experimental model of smoke inhalation injury in sheep, in which the same pathophysiologic alterations occur as with clinical inhalation in man, is described. Both the patients and the experimental sheep develop diffuse pulmonary mucosal sloughing, pulmonary edema and a decrease in systemic O2 tension. The pulmonary edema is apparently the result of an increase in microvascular permeability, characterized by increases in lung lymph flow (Qlym), lymph-to-plasma protein concentration ratio (L/P), and transvascular protein flux (Qlym .times. lung lymph protein concentration), while pulmonary vascular pressures remain constant. Neutrophil degranulation may contribute to the increased microvascular permeability.