Mitochondrial respiratory function as indicator of the ischemic injury of the rat kidney.
The function of mitochondria was considered to be an indicator of ischemic injury of the rat kidney, and the respiration of isolated mitochondria was measured in different metabolic states. The respiratory control index (RCI) was chosen as a parameter of mitochondrial intactness. The results indicate that normothermic in vitro ischemia leads to a rapid decrease of RCI and an almost complete loss of respiratory control within 45 min. Hypothermia during ischemic exposure proved to be an effective protection against mitochondrial injury as indicated by a prolonged coupled respiration and an RCI of about 2, even after 24 h of ischemic kidney storage. The ischemia-induced decrease of RCI was mainly due to a progressive decrease of active-state respiration, whereas the alterations of resting-state respiration were only small. The decline of active-state respiration was paralleled by a decrease of an uncoupled respiration rate. After termination of in vivo ischemia the RCI increased very slowly. Normal RCI values were not obtained until 7 days after onset of blood reflow, which supports the assumption of long-term damage due to ischemia.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D066298:In Vitro Techniques; D007511:Ischemia / Q000378:metabolism*; D007672:Kidney Cortex / Q000098:blood supply* / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D013696:Temperature; D013997:Time Factors
D000255:Adenosine Triphosphate