The effect of smoke inhalation on bradykinin metabolism by the perfused and ventilated rat lung.

Abstract

The effect of smoke inhalation on bradykinin metabolism was studied in the rat lung perfused with Ringer's bicarbonate solution. After smoke (from cotton, polyester, or seat cushion material) inhalation, tritium-labeled bradykinin was added to the Ringer's bicarbonate solution, and then the lung perfusion effluent aliquots containing bradykinin and its metabolic fragments were collected after a single transpulmonary passage. For the 20 control rats without smoke inhalation, 91% of the bradykinin dose was metabolized, with Pro-Pro (I), 49%, and Arg-Pro-Pro-Gly-Phe (II), 32%, being the predominant bradykinin cleavage fragments. For 12 rats with smoke inhalation, 89% of the bradykinin dose was metabolized, with I (28%) and II (36%) being the major bradykinin cleavage fragments. The type of smoke did not significantly alter the capacity of the rat lung to metabolize bradykinin. Exposure to smoke from seat cushion material for more than 3 minutes caused pulmonary edema and thickening, and smoke exposure for more than 5 minutes caused loss of integrity at the lung alveolar-capillary interface. In contrast, exposure to cotton or polyester smoke did not cause any observable gross changes of the lung. Electron microscopic examination of lung exposed to seat cushion material smoke revealed considerable damage, with the type I epithelium existing as patches on the alveolar surface and capillary endothelium separated from the basement lamina. Thus in our model acute, short-term inhalation of smoke did not significantly alter the amount of bradykinin metabolized by the pulmonary endothelium so long as the integrity of the lung alveolar-capillary interface was maintained, although there seemed to be a moderate shift in the amount of major cleavage fragments from I to II.