Pharmacological preconditioning effect of isoflurane against renal ischemia/reperfusion injury in rats.

异氟醚在心脏和大脑中具有药理预处理作用。在本研究中，我们对肾脏及其机制进行了探讨。将大鼠分为4组，每组8只。A、B组为假手术。C、D组双侧肾缺血40 min。B组和D组在假手术或缺血前给予1.5%异氟醚治疗20 min。分别于再灌注后12、24、48小时采血。血清肌酐和尿素氮在24和48 h时显著高于D组（p<0.01）。此外，在组织病理学检查中，可以看到异氟醚治疗对损伤的抑制。为探讨其作用机制，ⅰ组和ⅱ组分别给予单侧肾缺血40分钟。II组缺血前给予1.5%异氟醚治疗20 min。测定JNK、p38和ERK的活性。ⅱ组JNK、ERK活性显著低于ⅰ组（p<0.05）。综上所述，异氟醚在缺血前给药对肾缺血再灌注损伤具有预处理作用。蛋白激酶JNK和ERK的抑制可能参与了这一机制。

Isoflurane had a pharmacological preconditioning effect in the heart and brain. In this study, we investigated about the kidney and the mechanism. Rats were divided into four groups (n=8 for each). In groups A and B were sham surgery. Groups C and D were subjected to 40-min bilateral renal ischemia. Groups B and D received 1.5 % isoflurane for 20 min before sham surgery or ischemia. Blood sampling was performed at 12,24 and 48 hrs after reperfusion. The values of serum creatinine and blood urea nitrogen showed significant increases in group C compared to D at 24 and 48 hrs (p<0.01). Additionally in the histopathological examination, suppression of the damage was seen with the isoflurane treatment. To investigate the mechanism, group I and II were subjected to 40-min unilateral renal ischemia. Group II received 1.5 % isoflurane for 20 min before ischemia. The activities of JNK, p38 and ERK were measured. The activities of JNK and ERK in group II were significantly lower than those in group I (p<0.05). In conclusion, isoflurane shows preconditioning effect against renal ischemia/reperfusion injury when administered before ischemia. Inhibition of the protein kinases, JNK and ERK, might be involved in the mechanisms.