Abstract

Energy depletion closely correlates with ischemia-reperfusion (I-R) injury in solid organs, but there has been no conclusion about the lungs that contain air. We investigated the alveolar state during cold storage and its relation to energy metabolism and I-R injury in an ex vivo rat lung model. The lung was deflated (DEF group) or inflated with either room air (RA group) or nitrogen (N(2) group) for 6 h at 4 degrees C, and reperfusion samples of buffer and bronchoalveolar lavage fluid (BALF) was collected (n = 6, each). Furthermore, the static lung compliance, the intrapulmonary high-energy phosphates, lactate, and pyruvate were measured. The pulmonary functions of the DEF and N(2) groups were significantly worse than those of the RA group. In the N(2) group, the intrapulmonary levels of energy charge and pyruvate/lactate ratio were significantly lower than those in the DEF and RA groups, whereas there were no significant differences between the DEF and RA groups. In the DEF group, total protein and lactate dehydrogenase (LDH) in the BALF were significantly higher whereas the static lung compliance was significantly lower compared with the N(2) and RA groups. We concluded that aerobic metabolism would be essential for attenuating I-R injury of the lung, and inflation of the alveoli would be necessary for avoiding mechanical damage during reexpansion.

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