Heat shock preconditioning on mitochondria during warm ischemia in rat livers

The aim of this study was to investigate the effects of stress tolerance from heat shock preconditioning on changes in mitochondrial functions during ischemia-reperfusion injury of the liver.

Rats were divided into a heat shock group (group HS) and a control group (group C). In group HS, rats received heat shock pretreatment 48 h prior to ischemia-reperfusion. Heat shock pretreatment was performed in a water bath at 42 degrees C for 15 min under general anesthesia. In group C, the same treatment was done with the water bath at 37 degrees C instead of at 42 degrees C. A 30-min warm ischemia by cramping the hepatoduodinal ligament (Pringle's maneuver) followed by a 60-min reperfusion was administered to all rats. Changes in membrane potential of hepatic mitochondria (MPM); mitochondrial respiratory function before ischemia (n = 5), after ischemia (n = 10), and after reperfusion (n = 10); and ATP recovery after reperfusion were compared between the groups.

After a 30-min ischemia, MPM in group C decreased significantly and did not recover even after reperfusion. On the other hand, MPM in group HS was maintained even after a 30-min ischemia and 60 min into reperfusion as well. The respiratory control ratio (RCR) of the mitochondria in group C decreased to as low as 5.06 +/- 0.72 after a 30-min ischemia, but in group HS, RCR was maintained near a normal level. The ATP level recovered significantly earlier in group HS than in group C after reperfusion.

Heat shock preconditioning of the liver protected mitochondria from loss of membrane integrity during ischemia and contributed to their ability to produce energy-rich phosphates during reperfusion.