Smith L J
J Lab Clin Med. 1983 Apr;101(4):629-40.
This study was designed to determine whether MP could prevent the BHT-induced damage to the cells comprising the alveolar capillary barrier. Lung injury was produced in mice with an intraperitoneal injection of BHT. MP, 30 mg/kg, or saline was given 1 and 2 days later. Type 1 cell and endothelial cell damage and the percentage of capillaries containing PMNs and platelets were determined by electron microscopic morphometry. The type 2 cell LI was determined by light microscopic autoradiography. After the BHT injection, type 1 cell and endothelial cell damage occurred simultaneously and preceded an increase in the type 2 cell LI. The administration of MP before the appearance of electron microscopic evidence of type 1 cell and endothelial cell injury decreased the type 1 cell damage 2 and 3 days after the BHT injection by 89% (p less than 0.01) and 86% (p less than 0.005), decreased the endothelial cell damage by 46% and 76% (p less than 0.02), and prevented the increase in the type 2 cell LI. However, the administration of MP after type 1 cell and endothelial cell damage failed to prevent further damage or to inhibit the type 2 cell LI. MP had no effect on the percentage of capillaries containing PMNs or platelets. Thus, in the BHT model of acute lung injury, MP can prevent type 1 cell and endothelial cell damage, but its effect depends on the amount of injury present when the corticosteroid is given.