中文摘要：

目的：探讨盐酸右美托咪定（Dex）对重症急性胰腺炎（SAP）大鼠自主神经活性和肠黏膜屏障的可能作用。方法：将24只大鼠随机分为对照组、SAP组和Dex组。对照组为假手术组,SAP组通过胰胆管逆行注射牛磺胆酸钠建立SAP模型,Dex组在建立SAP模型后持续静脉输注Dex注射液。持续监测大鼠心率变异性（HRV）,观察自主神经功能的变化。用蛋白质印迹法检测小肠黏膜组织紧密连接蛋白Occludin和ZO-1的表达。用ELISA法检测肠黏膜炎性因子TNF-α和IL-6的表达。在造模后4、8和12 h抽血,用ELISA法检测血清肠脂肪酸结合蛋白（i FABP）变化。通过肠黏膜组织髓过氧化物酶（MPO）活性评估肠道中性粒细胞活性,通过丙二醛（MDA）水平评估肠道脂质氧化应激水平。结果：SAP组大鼠HRV明显降低,Dex组大鼠HRV明显高于SAP组。Dex能降低SAP大鼠肠黏膜炎性因子、MPO和MDA水平,上调紧密连接蛋白ZO-1的表达。并且,Dex组大鼠血清i FABP水平明显低于SAP组。结论：Dex能降低SAP大鼠交感神经活性,减轻肠黏膜损伤。

英文摘要：

Objective： To investigate the effects of dexmedetomidine （Dex） administration on intestinal mucosal barrier function in severe acute pancreatitis （SAP） rats. Methods： Twenty-four SD rats were randomly assigned to three groups： control group, SAP or Dex group. In Dex group, after modeling, rats received continuously intravenous pumping of Dex （5 μg/kg, h） for 12 hours. The changes of heart rate variability （HRV） were monitored continuously. The concentrations of occludin and ZO-1 in gut were detected by western-blotting. Intestinal TNF-α and IL-6 levels were investigated by ELISA. Femoral arterial blood was taken at 4 h, 8 h and 12 h after modeling for iFABP detections. Myeloperoxidase （MPO） and malondialdehyde （MDA） were also measured to study intestinal neutrophil accumulation and lipid peroxidation. Results： HRV levels were significantly lower in SAP group as compared with control group. Moreover, Dex could suppress the decrease in HRV in SAP rats. IL-6 and TNF-α levels, MPO and MDA in rat intestinal tissues and serum iFABP levels were markedly enhanced after SAP. Dex significantly decreased serum iFABP levels of SAP rats, as well as suppressed SAP-induced elevation of TNF-α, IL-6, MPO and MDA and increased ZO-1 expression in intestinal tissue. Conclusion： Dexmedetomidine could inhibit sympathetic activation and ameliorate intestinal mucosal barrier function in severe acute pancreatitis rats.