Rhodes R S, DePalma R G, Druet R L
Surg Gynecol Obstet. 1977 Nov;145(5):719-24.
To clarify the reversibility of ischemically induced mitochondrial dysfunction, a murine model of hepatic ischemia was used. Following 60 minutes ischemia to one hepatic lobe, significant alterations in mitochondrial, energy-linked metabolism were apparent. After the ischemic episode, 30 minutes of reperfusion resulted in partial restoration of mitochondrial function with succinate but not alpha-ketoglutarate as substrate. Lactate accumulation was also partially reversed with reperfusion. Histologic examination subsequent to the ischemic episode revealed development of partial necrosis in nine of ten ischemic lobes. alpha-Ketoglutarate oxidation is more sensitive to injury than succinate oxidation. With proper choice of substrate, measurement of mitochondrial function just after an ischemic insult may predict subsequent hepatic failure due to cellular necrosis.
为阐明缺血诱导的线粒体功能障碍的可逆性，使用了肝缺血的小鼠模型。对一个肝叶进行60分钟缺血后，线粒体能量相关代谢出现明显改变。缺血发作后，30分钟的再灌注导致以琥珀酸而非α-酮戊二酸为底物时线粒体功能部分恢复。再灌注也使乳酸积累部分逆转。缺血发作后的组织学检查显示，十个缺血肝叶中有九个出现部分坏死。α-酮戊二酸氧化比琥珀酸氧化对损伤更敏感。通过适当选择底物，在缺血损伤后立即测量线粒体功能可能预测随后因细胞坏死导致的肝衰竭。
