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目的：肝脏缺血再灌注肝损伤的机理尚未清楚。本研究通过观察大鼠肝缺血和再灌注后血浆内皮素（ＥＴ１）、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆｌａ、ＳＧＰＴ和病理变化，了解ＥＴ１在肝热缺血再灌注肝损伤中的作用。方法：ＳＤ大鼠３２只分为４组：正常对照组，肝缺血组，再灌注后３０ｍｉｎ和４ｈ组。通过用无损伤动脉夹阻断肝蒂造成大鼠肝缺血动物模型。经腹主动脉采血用放射免疫方法检测血浆ＥＴ１、ＴＸＢ２、６－Ｋｅｔｏ－ＰＧｌａ，同时检测ＳＧＰＴ。统计学方法：ｑ检验，回归相关分析和ｔ检验。结果：肝缺血再灌注导致ＥＴ１和ＳＧＰＴ明显增高（Ｐ＜０．０５），并伴随以６－Ｋｅｔｏ－ＰＧｌａ）增高为主的ＴＸＢ２／６－ｋｅｔｏ－ＰＧＩａ比值失调，这种变化在再灌注４ｈ时尤为明显。此时６－Ｋｅｔｏ－ＰＧＦｌａ与ＥＴ１变化呈正相关，相关系数ｒ＝０．７９（Ｐ＜０．０５）。结论：ＥＴ１是参与肝热缺血及再灌注后肝损伤的主要因素之一，其作用可能是导致肝微循环障碍而加重肝继发性损害
Objective: The mechanism of hepatic ischemia-reperfusion injury in liver is not yet clear. In this study, ET1, TXB2, 6-keto-prostaglandin Fla, SGPT and pathological changes were observed after hepatic ischemia and reperfusion in rats to understand the role of ET1 in hepatic ischemia-reperfusion liver The role of injury. Methods: 32 SD rats were divided into 4 groups: normal control group, hepatic ischemia group, 30 min and 4 h after reperfusion. Animal model of hepatic ischemia in rats was established by blocking the pedicle with an intact arterial clip. Blood samples were collected from the abdominal aorta by radioimmunoassay to detect plasma ET1, TXB2, 6-Keto-PGla and detect SGPT. Statistical methods: q test, regression analysis and t test. Results: The hepatic ischemia / reperfusion resulted in the imbalance of TXB2 / 6-keto-PGIa with ET1 and SGPT significantly increased (P <0.05) and accompanied with the increase of 6-Keto-PGla. This change in reperfusion 4h is especially obvious. There was a positive correlation between 6-Keto-PGFla and ET1 (r = 0.79, P <0.05). Conclusion: ET1 is one of the main factors involved in hepatic injury after hepatic ischemia and reperfusion, and its role may be to cause hepatic microcirculation disturbance and aggravate secondary hepatic injury