Mitochondrial respiration as an early marker of viability in cardiac-arrested rat lungs.

BACKGROUND

To evaluate the possibility of using pulmonary mitochondrial respiratory functions as early markers of ischemic lung viability in non-heart-beating donors, we investigated the roles of the mitochondria in ischemia-reperfusion injury of cardiac-arrested rat lungs.

MATERIALS AND METHODS

Male Lewis rats were exposed to various periods of postmortem warm ischemia (0, 1, and 2 h at 21 degrees C). After a pulmonary artery flush and cold preservation (1 h at 4 degrees C), the rat lungs were reperfused using an isolated rat lung model. Each experimental group consisted of three subgroups (n = 7 in each subgroup) to examine pulmonary functions and biochemical measurements.

RESULTS

The pulmonary functions after reperfusion were exacerbated after a 1-h postmortem warm ischemia and worsened after a 2-h warm ischemia following cardiac arrest. The mitochondrial respiratory control ratios already significantly decreased after a 1-h warm ischemia compared with nonischemic rat lungs, at which time the value was almost equivalent to that after a 2-h ischemia. There were no significant changes in the state 3 and 4 respiration of the mitochondria, the pulmonary lactate levels, or the lipid peroxide levels in the lung tissues and mitochondria during the first 1-h period of warm ischemia. The adenine nucleotide levels significantly decreased with the prolongation of the period of warm ischemia, but did not seem to be practical, because their determination required a much longer time than that of the mitochondrial respiratory control ratio.

CONCLUSION

These results suggested that the mitochondrial respiratory control ratio may be a useful early marker for lung viability after cardiac arrest.