Lee H Thomas, Ota-Setlik Ayuko, Fu Yulei, Nasr Samih H, Emala Charles W
Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, New York, USA.
Anesthesiology. 2004 Dec;101(6):1313-24. doi: 10.1097/00000542-200412000-00011.
Volatile anesthetics protect against cardiac ischemia-reperfusion injury via adenosine triphosphate-dependent potassium channel activation. The authors questioned whether volatile anesthetics can also protect against renal ischemia-reperfusion injury and, if so, whether cellular adenosine triphosphate-dependent potassium channels, antiinflammatory effects of volatile anesthetics, or both are involved.
Rats were anesthetized with equipotent doses of volatile anesthetics (desflurane, halothane, isoflurane, or sevoflurane) or injectable anesthetics (pentobarbital or ketamine) and subjected to 45 min of renal ischemia and 3 h of reperfusion during anesthesia.
Rats treated with volatile anesthetics had lower plasma creatinine and reduced renal necrosis 24-72 h after injury compared with rats anesthetized with pentobarbital or ketamine. Twenty-four hours after injury, sevoflurane-, isoflurane-, or halothane-treated rats had creatinine (+/- SD) of 2.3 +/- 0.7 mg/dl (n = 12), 1.8 +/- 0.5 mg/dl (n = 6), and 2.4 +/- 1.2 mg/dl (n = 6), respectively, compared with rats treated with pentobarbital (5.8 +/- 1.2 mg/dl, n = 9) or ketamine (4.6 +/- 1.2 mg/dl, n = 8). Among the volatile anesthetics, desflurane demonstrated the least reduction in plasma creatinine after 24 h (4.1 +/- 0.8 mg/dl, n = 12). Renal cortices from volatile anesthetic-treated rats demonstrated reduced expression of intercellular adhesion molecule 1 protein and messenger RNA as well as messenger RNAs encoding proinflammatory cytokines and chemokines. Volatile anesthetic treatment reduced renal cortex myeloperoxidase activity and reduced nuclear translocation of proinflammatory nuclear factor kappaB. Adenosine triphosphate-dependent potassium channels are not involved in sevoflurane-mediated renal protection because glibenclamide did not block renal protection (creatinine: 2.4 +/- 0.4 mg/dl, n = 3).
Some volatile anesthetics confer profound protection against renal ischemia-reperfusion injury compared with pentobarbital or ketamine anesthesia by attenuating inflammation. These findings may have significant clinical implications for anesthesiologists regarding the choice of volatile anesthetic agents in patients subjected to perioperative renal ischemia.
挥发性麻醉药通过激活三磷酸腺苷依赖性钾通道来预防心脏缺血-再灌注损伤。作者质疑挥发性麻醉药是否也能预防肾缺血-再灌注损伤，如果可以，细胞三磷酸腺苷依赖性钾通道、挥发性麻醉药的抗炎作用或两者是否都参与其中。
用等效剂量的挥发性麻醉药（地氟烷、氟烷、异氟烷或七氟烷）或注射用麻醉药（戊巴比妥或氯胺酮）麻醉大鼠，并在麻醉期间使其经历45分钟的肾缺血和3小时的再灌注。
与用戊巴比妥或氯胺酮麻醉的大鼠相比，用挥发性麻醉药治疗的大鼠在损伤后24 - 72小时血浆肌酐水平较低，肾坏死减少。损伤后24小时，七氟烷、异氟烷或氟烷治疗的大鼠肌酐（±标准差）分别为2.3±0.7mg/dl（n = 12）、1.8±0.5mg/dl（n = 6）和2.4±1.2mg/dl（n = 6），而戊巴比妥治疗的大鼠为5.8±1.2mg/dl（n = 9），氯胺酮治疗的大鼠为4.6±1.2mg/dl（n = 8）。在挥发性麻醉药中，地氟烷在24小时后血浆肌酐降低最少（4.1±0.8mg/dl，n = 12）。挥发性麻醉药治疗的大鼠肾皮质中细胞间黏附分子1蛋白和信使核糖核酸以及编码促炎细胞因子和趋化因子的信使核糖核酸表达降低。挥发性麻醉药治疗降低了肾皮质髓过氧化物酶活性，并减少了促炎核因子κB的核转位。三磷酸腺苷依赖性钾通道不参与七氟烷介导的肾保护，因为格列本脲未阻断肾保护作用（肌酐：2.4±0.4mg/dl，n = 3）。
与戊巴比妥或氯胺酮麻醉相比，一些挥发性麻醉药通过减轻炎症对肾缺血-再灌注损伤具有显著的保护作用。这些发现可能对麻醉医生在接受围手术期肾缺血的患者中选择挥发性麻醉药具有重要的临床意义。
