Heat shock preconditioning on mitochondria during warm ischemia in rat livers

Citation
Y. Ishikawa et al., Heat shock preconditioning on mitochondria during warm ischemia in rat livers, J SURG RES, 87(2), 1999, pp. 178-184
Citations number
46
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF SURGICAL RESEARCH
ISSN journal
00224804 → ACNP
Volume
87
Issue
2
Year of publication
1999
Pages
178 - 184
Database
ISI
SICI code
0022-4804(199912)87:2<178:HSPOMD>2.0.ZU;2-A
Abstract
Background. The aim of this study was to investigate the effects of stress tolerance from heat shock preconditioning on changes in mitochondrial funct ions during ischemia-repel fusion injury of the liver. Materials and methods. Rats were divided into a heat shock group (group HS) and a control group (group C), In group HS, rats received heat shock pretr eatment 48 h prior to ischemia-reperfusion. Heat shock pretreatment was per formed 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 hepato duodinal ligament (Pringle's maneuver) followed by a 60-min reperfusion was administered to all rats. Changes in membrane potential of hepatic mitocho ndria (MPM); mitochondrial respiratory function before ischemia (n = 5), af ter ischemia (n = 10), and after reperfusion (n = 10); and ATP recovery aft er reperfusion were compared between the groups. Results. After a 30-min ischemia, MPM in group C decreased significantly an d did not recover even after reperfusion, On the other hand, MPM in group H S was maintained even after a 30-min ischemia and 60 min into reperfusion a s 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 signifi cantly earlier in group HS than in group C after reperfusion, Conclusions. Heat shock preconditioning of the liver protected mitochondria from loss of membrane integrity during ischemia and contributed to their a bility to produce energy-rich phosphates during reperfusion, a 1999 Academi c press.