REVERSIBILITY OF ISCHEMICALLY INDUCED MITOCHONDRIAL DYSFUNCTION WITH REPERFUSION

  • 1 January 1977
    • journal article
    • research article
    • Vol. 145  (5) , 719-724
Abstract
To clarify the reversibility of ischemically induced mitochondrial dysfunction, a murine [rat] model of hepatic ischemia was used. Following 60 min ischemia to 1 hepatic lobe, significant alterations in mitochondrial, energy-linked metabolism were apparent. After the ischemic episode, 30 min of reperfusion resulted in partial restoration of mitochondrial function with succinate, but not .alpha.-ketoglutarate, as substrate. Lactate accumulation was partially reversed with reperfusion. Histologic examination subsequent to the ischemic episode revealed development of partial necrosis in 9 of 10 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.