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.


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.


CONCLUSIONS
These results suggested that the mitochondrial respiratory control ratio may be a useful early marker for lung viability after cardiac arrest.
Hirata
T
T
Department of Thoracic Surgery, Kyoto University, Kyoto, 606-8397, Japan.
Fukuse
T
T
Hanaoka
S
S
Matsumoto
S
S
Chen
Q
Q
Wada
H
H
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D015415:Biomarkers; D006324:Heart Arrest, Induced; D006358:Hot Temperature; D007511:Ischemia / Q000503:physiopathology; D019344:Lactic Acid / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008928:Mitochondria / Q000378:metabolism* / Q000502:physiology; D010101:Oxygen Consumption; D011652:Pulmonary Circulation; D051381:Rats; D011917:Rats, Inbred Lew; D014022:Tissue Survival
D000227:Adenine Nucleotides; D015415:Biomarkers; D008054:Lipid Peroxides; D019344:Lactic Acid