Interaction between anesthetic agents and ischemic preconditioning in hepatoenteric ischemia reperfusion injury.

本研究旨在探讨麻醉剂与ATP依赖性钾通道激活的相互作用及肝内脏缺血预处理的保护作用。建立兔部分肝缺血再灌注模型，采用微血管血流量和半乳糖清除率测定肝缺血再灌注损伤。首先，我们发现异氟烷，挥发性麻醉剂，提供更强的保护相比，静脉麻醉剂，丙泊酚（美国社会麻醉学家，年度会议A-94，2002）。其次，尼可地尔激活ATP依赖性钾通道在肝脏缺血性损伤中没有提供显著的保护作用（美国麻醉学家学会，年会A-721，2003）。这些结果正在提交或处于准备阶段，以便将来提交给英文学术期刊。此外，预处理和抑制中性粒细胞或枯否细胞依赖的炎症过程之间的相互作用正在研究中。

In this research project, the interaction between anesthetic agents as well as ATP-dependent potassium channel activation and protective effects caused by ischemic preconditioning in hepatosplanchnic organs. We established the partial hepatic ischemia-reperfusion model in anesthetized rabbits and determined the hepatic ischemia-reperfusion injury with microvascular blood flow and galactose clearance. First, we found that isoflurane, volatile anesthetic agent, offered stronger protection compared to intravenous anesthetic, propofol (Am Soc Anesthesiologists, annual meeting A-94, 2002). Second, activation of ATP-dependent potassium channel by nicorandil did not offer signiftcant protection in the liver ischemic injury (Am Soc Anesthesiologists, annual meeting A-721, 2003). These results are either under submission or during preparatory phase for future submission to the English academic journals. Furthermore, the interaction between preconditioning and suppression of neutrophil or Kupffer cell-dependent inflammatory process are under investigation.