ATTENUATION OF WARM ISCHEMIC INJURY OF RAT LUNG BY INFLATION WITH ROOM AIR-ASSESSMENT OF CELLULAR COMPONENTS AND THE SURFACTANT IN THE BRONCHOALVEOLAR LAVAGE FLUID IN RELATION TO CHANGES IN CELLULAR ADENOSINE TRIPHOSPHATE
Studies were made on the effects in rat lungs of aerobic and anaerobic conditions on the intracellular levels of adenosine triphosphate and its related metabolites, the releases of intracellular enzymes, and the secretion of pulmonary surfactant. After warm ischemia for 120 min, the ATP content of lungs inflated with air was significantly higher (8.0±1.2 μmol/g dry weight) than those of deflated lungs and lungs inflated with nitrogen (0.8±0.7 μmol/g dry weight and 2.0±0.7 μmol/g dry weight, respectively; P<0.001). The amounts of intracellular enzymes, such as lactate dehydrogenase, cyto-solic and mitochondrial aspartate aminotransferase, and protein in the bronchoalveolar lavage fluid (BALF) of air-inflated lungs were significantly less than those in BALFs of deflated and nitrogen-inflated lungs (P<0.001). The BALF-contents of dipalmitoyl phosphatidylcholine (DPPC), the main component of alveolar surfactant of aerobic and anaerobic ischemic lung were, however, similar. During 120-min warm ischemia after lavage, air-inflated lungs secreted significantly more DPPC into the alveolar space than nitrogen-inflated lungs did (P<0.001). We conclude that cell membranes in the lungs are damaged under anaerobic conditions, but that inflation of ischemic lungs with air is effective for protecting them from cell injury and for maintaining the intracellular level of ATP and the ability of the cells to secrete pulmonary surfactant.