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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。
Objective: To investigate the possible effect of dexmedetomidine hydrochloride on autonomic nerve activity and intestinal mucosal barrier in severe acute pancreatitis (SAP) rats. Methods: 24 rats were randomly divided into control group, SAP group and Dex group. The control group was sham-operation group. In the SAP group, SAP model was established by retrograde injection of sodium taurocholate into the SAP group. Dex group was infused with Dex injection continuously after SAP model was established. The heart rate variability (HRV) of rats was continuously monitored to observe the changes of autonomic nervous function. Western blotting was used to detect the expression of tight junction proteins Occludin and ZO-1 in intestinal mucosa. The expressions of inflammatory factors TNF-α and IL-6 in intestinal mucosa were detected by ELISA. Blood samples were taken at 4, 8 and 12 h after model establishment, and the changes of serum intestinal fatty acid binding protein (i FABP) were detected by ELISA. Intestinal neutrophil activity was assessed by myeloperoxidase (MPO) activity in intestinal mucosa and intestinal oxidative stress was assessed by malondialdehyde (MDA) levels. Results: HRV in SAP group was significantly lower than that in SAP group. HRV in Dex group was significantly higher than that in SAP group. Dex can reduce the intestinal mucosal inflammatory factor, MPO and MDA in SAP rats and up-regulate the expression of tight junction protein ZO-1. Moreover, serum i FABP level in Dex group was significantly lower than that in SAP group. Conclusion: Dex can reduce the sympathetic activity of SAP rats and relieve the intestinal mucosal damage.