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作 者:胡永奇[1] 张连元[1] 李宏杰[1] 彭军[1] 董淑云[1] 门秀丽[1] 杨全会[1] 周红霞[1]
机构地区:[1]华北煤炭医学院病理生理教研室,河北唐山063000
出 处:《中国应用生理学杂志》2005年第1期30-33,共4页Chinese Journal of Applied Physiology
摘 要:目的 :研究一氧化氮 (NO)和内皮素 1(ET 1)在大鼠肢体缺血 /再灌注 (LI/R)后脑损伤中的作用 ,探讨NO/ET 1平衡关系的变化对脑损伤的影响。方法 :在大鼠LI/R损伤模型上 ,应用NO合成前体物质L 精氨酸 (L Arg)、一氧化氮合酶 (NOS)抑制剂氨基胍 (AG)、ETA 受体阻断剂BQl2 3进行干预 ,观察血浆NO、ET 1、MDA、XOD、SOD、LDH及脑组织tNOS、iNOS、cNOS、NO、ET 1、MDA、XOD、MPO、SOD的变化。结果 :与对照组比较 ,I/R组血浆MDA、XOD、LDH及脑组织MDA、XOD、MPO升高 ,SOD活性降低 (P <0 .0 1) ,脑组织tNOS和iNOS明显升高 ,而cNOS明显降低 (P <0 .0 1) ,I/R组血浆及脑组织NO、ET 1增加 ,NO/ET 1比值降低 ,脑损伤加重。应用L Arg及BQ12 3后 ,血浆及脑组织NO/ET 1比值较I/R组升高 ,脑损伤减轻 ,应用AG后 ,NO/ET 1比值降低 ,脑损伤进一步加重。结论 :肢体缺血 /再灌注后 ,一氧化氮与内皮素 l的比值降低时脑损伤加重。Aim: To study the roles of nitric oxide(NO) and ET-1 in brain injury after hind limbs ischemia/reperfusion in rats and to investigate the effect of NO/ ET-1 balance on brain injury. Methods: On a model of the hind limbs ischemia/reperfusion(LI/R) of rats, we used L-Arg(L-arginine,L-Arg), one of the substrates in the process of nitric oxide, aminoguanidine(AG) which inhibits nitric oxide synthase(NOS) and ET A receptor antagonist BQ123, to observe the changes of NO, ET-1, MDA, XOD, SOD, LDH in plasma and tNOS, iNOS, cNOS, NO, ET-1, MDA, XOD, MPO, SOD in brain tissue. Results: Compared with the control group, the content of MDA, XOD, LDH in plasma and MDA, XOD, MPO in brain tissue increased. The activity of SOD decreased(P< 0.01 ). The content of tNOS, iNOS in brain tissue increased, cNOS decreased(P<0.01).The content of NO, ET-1 in I/R group in plasma and brain tissue increased, the ratio of NO/ET-1 decreased. The brain injury was deteriorated. After using L-Arg and BQ123, the ratio of NO/ET-1 in plasma and brain tissue increased, the brain injury lightened. Whereas after using AG, the ratio of NO/ET-1 decreased,brain injury became more serious. Conclusion: The NO/ET-1 ratio decreased after LI/R, brain injury became more serious.
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