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采用静脉注射脂多糖(lipopolysaccharide,LPS)的方法建立小鼠内毒素休克模型,探讨内毒素休克时小肠微循环的变化以及诱导型一氧化氮合酶(iNOS)对小肠微循环的影响。实验过程中连续监测小鼠平均动脉血压(meanarterialpressure,MAP)变化情况。利用FITC标记红细胞和活体显微镜方法直接观察并计算小鼠小肠绒毛尖端小动脉和毛细血管内红细胞的流速和流量,并观察敲除小鼠iNOS基因和选择性iNOS抑制剂S-methylthioureasulfate(SMT)对实验过程中小肠微循环的影响。结果显示,对于野生型小鼠,应用SMT处理和敲除iNOS基因对基线的MAP、小肠绒毛尖端小动脉和毛细血管的红细胞流速和流量没有显著性差别。给予LPS后,小鼠的MAP进行性下降。给予LPS前,应用SMT和敲除小鼠iNOS基因可以显著提高MAP;给予LPS后,小鼠小肠绒毛尖端小动脉和毛细血管内红细胞流速和流量显著下降。给予LPS前,应用SMT和敲除小鼠iNOS基因可以显著提高小肠绒毛尖端小动脉和毛细血管的红细胞流速和流量。结果表明,iNOS在内毒素休克小肠微循环衰竭的过程中发挥重要作用。
The model of endotoxic shock in mice was established by intravenous injection of lipopolysaccharide (LPS). The changes of small intestine microcirculation and the effect of inducible nitric oxide synthase (iNOS) on microcirculation of small intestine were investigated. During the experiment, mean arterial blood pressure (MAP) changes were monitored continuously. FITC-labeled erythrocytes and in vivo microscopy were used to directly observe and calculate the flow velocity and flow rate of mouse small intestine villous arterioles and capillary erythrocytes. The knockout mice iNOS gene and the selective iNOS inhibitor S-methylthioureasulfate (SMT) Effect of microcirculation in small intestine during the experiment. The results showed that there was no significant difference in the flow rate and flux of erythrocytes between the MAP and the intestinal villi tip arterioles and capillaries of the wild-type mice treated with SMT and knock-out of the iNOS gene. After LPS administration, the MAP of mice decreased progressively. Before administration of LPS, the application of SMT and knockout mice iNOS gene can significantly improve the MAP; LPS, the mouse small intestine villi tip arterioles and capillary erythrocyte flow rate and flow decreased significantly. Application of SMT and knockout of mouse iNOS gene significantly increased erythrocyte flow and flux in small intestine villous arterioles and capillaries prior to LPS administration. The results showed that iNOS play an important role in the process of endotoxic shock and intestinal microcirculation failure.