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目的建立脾静脉-股静脉转流下大鼠全肝缺血再灌注损伤模型。方法 40只Wistar 大鼠,体重240-270 g,随机分为2组:单纯肝门阻断组(C组);脾静脉-股静脉转流下肝门阻断组(B 组),应用自制转流泵调节转流量在5-10ml·min-1。两组均用无创动脉夹夹闭肝动脉、门静脉及胆总管40min,随后放开动脉夹再灌注。监测缺血前即刻、缺血5、10、40min及再灌注5、20 min时平均动脉压(MAP)、中心静脉压(CVP)、门静脉压(PVP)、心率(HR)、心电图和胃肠淤血情况,观察再灌注1、24 h肝脏、小肠的病理改变及再灌注24 h的存活率。结果与缺血前即刻比较,C组缺血观察40min、再灌注20min时MAP降低,缺血10、40min时CVP降低,再灌注5、20min时CVP升高,缺血5-40 min、再灌注5、20 min时PVP升高,缺血10、40 min、再灌注5、20min时HR升高;B组缺血5-40 min、再灌注5 min时MAP下降,缺血10 min时PVP升高,缺血5 min时HR下降(P<0．05或0．01)。与C组比较,B 组缺血5-40min、再灌注5、20 min时MAP、PVP,缺血10、40min、再灌注5、20 min时CVP,再灌注5、20 min时HR差异有统计学意义,心律失常发生率降低,再灌注24 h存活率升高(P<0．05或0．01)。B组无明显的胃肠淤血。与C组比较,再灌注1 h B组只有少部分肠绒毛顶端有变性脱落,粘膜下炎症不明显,两组肝脏病理均可见肝小叶结构完整,中央静脉及肝窦扩张,汇管区炎症浸润;再灌注24 h时C 组可见肝细胞点片状坏死,B组多为点状肝细胞坏死。结论大鼠脾静脉-股静脉转流下全肝缺血再灌注损伤模型血液动力学稳定,腹腔内脏器无淤血,无肠道屏障破坏。
Objective To establish a rat model of total hepatic ischemia-reperfusion injury after splenic vein-femoral vein bypass. Methods Forty Wistar rats, weighing 240-270 g, were randomly divided into two groups: simple hepatic hilar block (group C), hepatic portal vein block (group B) with splenic vein-femoral vein bypass, Flow pump to regulate the flow in the 5-10ml · min-1. Both groups were noninvasive artery clip clamping hepatic artery, portal vein and common bile duct 40min, then release the artery clip reperfusion. The mean arterial pressure (MAP), central venous pressure (CVP), portal pressure (PVP), heart rate (HR), electrocardiogram and gastrointestinal Congestion, observe the pathological changes of liver and small intestine 1,24 h after reperfusion and the survival rate of 24 h after reperfusion. Results Compared with the time before ischemia, MAP was observed in group C at 40 min and at 20 min after reperfusion. CVP was decreased at 10 min and 40 min. CVP was increased at 5 min and 20 min, PVP increased at 5 and 20 min, HR increased at 10 min, 40 min and 5 min and 20 min after reperfusion. In group B, the MAP decreased at 5-40 min and 5 min after reperfusion, while PVP increased at 10 min after ischemia HR, HR decreased 5 min after ischemia (P <0.05 or 0.01). Compared with group C, there were statistical differences in HR between 5-40 minutes after ischemia, MAP, PVP at 5,20 minutes after reperfusion, 10,40 minutes after ischemia, CVP at 5,20 minutes after reperfusion and 5,20 minutes after reperfusion Significance, the incidence of arrhythmia decreased, and the survival rate increased 24 h after reperfusion (P <0.05 or 0.01). B group without obvious gastrointestinal congestion. Compared with group C, only a few of villus villus degeneration and submucosal inflammation were not observed in group B at 1 h after reperfusion. The structure of hepatic lobules, the dilatation of central venous and hepatic sinusoids and inflammatory infiltration in portal area were observed in both groups. At 24 hours after reperfusion, hepatocyte lamellar necrosis was observed in group C, and punctate hepatocyte necrosis in group B was observed. Conclusions The model of hepatic ischemia-reperfusion injury in rats with splenic vein-femoral vein bypass is stable in hemodynamics, with no congestion in the abdominal organs and no barrier damage to the intestine.