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作 者:徐竞[1] 蓝丹[1] 李涛[1] 杨光明[1] 刘良明[1]
机构地区:[1]第三军医大学大坪医院野战外科研究所二室创伤,烧伤与复合伤国家重点实验室,邮政编码重庆400042
出 处:《微循环学杂志》2012年第1期6-9,I0001,共5页Chinese Journal of Microcirculation
基 金:国家自然科学基金(No.30801189);重庆市自然科学基金(CSTC;2008BB5103)
摘 要:目的:观察诱导型一氧化氮合酶(iNOS)在血管生成素-1(Ang-1)、血管生成素-2(Ang-2)调节失血性休克大鼠血管反应性双相变化中的作用。方法:采用WesternBlotting观察iNOS蛋白表达,同时采用离体微血管环张力测定技术检测血管反应性,以及细胞一氧化氮(NO)含量。结果:iNOS表达在失血性休克后逐渐增高;iNOS抑制剂可显著恢复缺氧4h的血管低反应性,抑制Ang-2进一步降低缺氧4h血管反应性的作用,去甲肾上腺素(NE)的最大收缩力(Emax)分别由5.875mN增高至8.937mN和由3.444mN增高至7.492mN(P<0.01);Ang-1,Tie-2、p38MAPK和Erk抑制剂可抑制缺氧4h的iNOS表达和增加NO生成(P<0.01)。结论:失血性休克晚期,Ang-1和Ang-2可通过p38MAPK和Erk调节iNOS蛋白表达,增加NO生成来调节血管低反应性。Objective:To observe the role of inducible nitricoxide synthase(iNOS) in the regulation of angiopoietin-1(Ang-1) and angiopoietin-2(Ang-2) on the biphasic change of vascular reactivity after hemorrhagic shock in rats.Method:The western blotting was adopted to observe the protein expression of iNOS,the microvascular tension determine technique was adopted to observe the vascular reactivity in vitro,the nitric oxide(NO) kit was adopted to measure the concentration of NO.Results:The protein expression of iNOS in SMA was increased significantly after 30min shock.Inhibitor of iNOS could improve the vascular reactivity in 4h hypoxia(the Emax of NE was increased from 5.875mN to 8.937mN,P<0.05),and repress the decreas effect of Ang-2 on vascular reactivity in 4h hypoxia(the Emax of NE was increased from 3.444mN to 7.492mN,P<0.01).The protein expression of iNOS and the concentration of NO in 4h hypoxia group was increased significantly as compared with normal control,which could be decreased by Ang-1,Tie-2,p38MAPK and Erk inhibitor(P<0.01).Conclusion:Ang-1 and Ang-1 regulate the vascular hyporeactivity in the late period of hemorrhagic shock in rats by changing the protein expression of iNOS and NO production through p38MAPK and Erk.
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