Early tissue damage in ethchlorvynol-induced alveolar edema in rabbit lung.

The purpose of this study was to examine the morphologic changes that occur in the early stages of intraalveolar edema. Anesthetized rabbits were intravenously administered a bolus of 40 mg/kg of ethchlorvynol, a mild hypnotic known to induce respiratory distress syndrome in humans and laboratory animals when given intravenously. After 15 min their lungs were fixed for transmission electron microscopy. Examination revealed variable amounts of irregularly distributed intraalveolar edema with erythrocytes and fibrin strands that coexisted with modest or nonexisting interstitial edema suggesting that primary hemorrhagic alveolar flooding had taken place. Most alveolar epithelial and endothelial cells appeared normal except in localized areas. In lungs fixed by vascular perfusion, in which normal capillaries were flushed, obstructions were noticed in alveolar corner capillaries. These areas were identified by light microscopy and selectively sectioned for electron microscopy. They contained intravascular cell-fibrin aggregates consisting of plugs of degranulated platelets, fibrin, erythrocytes, and leukocytes. Endothelial and epithelial cells in the vicinity of the plugs showed variable degrees of injury. In places the damage was so severe that vascular and alveolar spaces were separated only by the basal lamina. Our work shows the previously unnoticed existence of capillary microemboli or microthrombi in a well-known experimental model of respiratory distress syndrome and suggests extravasation of blood elements through discrete sites of cell injury associated with the fibrin-platelet aggregates rather than diffuse increase of permeability as cause of early alveolar flooding.