Study of mechanism and condition for ischemic preconditioning induced by volatile anesthetics pretreatment in the liver

挥发性麻醉药预处理引起肝脏缺血预适应的机制和条件研究

• 批准号: 12470314
• 负责人: INABA Hideo
• 金额: $ 6.02万
• 依托单位: Kanazawa University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-12470314/
• 关键词: volatile anesthetics; ischemic preconditioning; isolated perfused liver; liver slice incubation; apoptosis; patch clamp; K-ATP channel; 虚血耐性; ATP感受性Kチャンネル; 肝臓; β細胞; K(ATP)チャンネル; ischemic preconditioning; 摘出臓器灌流; 内皮細胞; 肺

Halothane, isoflurane and sevoflurane attenuated ischemia-reperfusion injury in the perfused liver of fasted rats, suggesting a possible involvement of ischemic preconditioning.In the rat liver slice incubation, isoflurane attenuated apoptosis induced by hypoxic challenge. Suppression of apoptosis is predominant in the hepatocyte.Direct effect of isoflurane on K-ATP channel was studied in isolated pancreatic β cells using whole cell patch clamp method. Isoflurane suppressed K-ATP channel in a dose-dependent manner. Repeated treatment of isoflurane enhanced the suppression of K-ATP channel.

氟烷、异氟醚和七氟醚均能减轻禁食大鼠肝脏缺血再灌注损伤，提示缺血预处理可能参与了这一过程。用全细胞膜片钳技术研究了异氟醚对胰腺β细胞K-ATP通道的直接作用。异氟醚呈剂量依赖性抑制K-ATP通道。异氟醚重复给药可增强对K-ATP通道的抑制作用。