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诱生型一氧化氮合酶mRNA的表达对心脏移植术后移植物血管病的抑制作用

Expression of iNOS mRNA prevented cardiac allograft vasculopathy after heart transplantation
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摘要 目的探讨诱导诱生型一氧化氮合酶(iNOS)mRNA的表达以促进NO合成对移植物血管病(CAV)形成的抑制作用。方法建立大鼠异位(腹部)心脏移植模型,受者在接受环孢素A腹腔注射的同时,按分组要求分别给予左旋精氨酸(iNOSmRNA组)、一氧化氮合酶(NOS)抑制剂左旋精氨酸甲酯(LNAME组),术后测定血浆NO3-的含量、移植心脏冠状血管iNOSmRNA的表达以及冠状动脉内膜与中膜厚度比的改变。结果术后2周和4周,iNOSmRNA组血浆NO3-的含量明显高于对照组和LNAME组,移植心脏组织中iNOSmRNA的表达水平高于对照组和LNAME组,而术后4周的冠状动脉内膜中膜厚度比显著低于对照组和LNAME组。结论iNOSmRNA的表达可以促进NO的大量合成,对心脏移植后的移植物血管病有一定的抑制作用。 Objective To study the prevention of cardiac allograft vasculopathy (CAV) post-transplant through the expression of iNOS mRNA. Methods Rat model of heterotopic heart transplantation (Abdomen) was developed and recipients were injected with Cyclosporin A at abdomen in the meantime of receiving L-arginine (iNOS mRNA group) and inhibitor of iNOS (L-NAME group) according to grouping. Plasma content of NO_3-, the expression of iNOS mRNA in coronary ~artery of transplanted heart and the radio of tunica intima/tunica media thickness (I/M) were assayed after ~operation . Results The plasma content of NO_3-and the expression of iNOS mRNA in coronary ~artery of transplanted heart in iNOS mRNA group were obviously higher than those in control group and L-NAME group during 2 to 4 weeks after operation. The ratio of I/M in iNOS mRNA group was ~lower than that in control group and L-NAME group 4 weeks after operation. Conclusion The ~expression of iNOS can promote the synthesis of NO and prevent CAV development.
出处 《中华器官移植杂志》 CAS CSCD 北大核心 2005年第1期50-52,共3页 Chinese Journal of Organ Transplantation
基金 国家自然科学基金资助项目(30300343)
关键词 心脏移植 移植物 心血管疾病 一氧化氮合酶 Heart transplantation Transplants Cardiovascular diseases Nitric-oxide synthase
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参考文献7

  • 1Mehra MR, Venture HO, Uber PA, et al. Is all intimal proliferation created equal in cardiac allograft vasculopathy? The quantity-quality paradox. J Heart Lung Transplant, 2003, 22: 118-123.
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  • 4Pinsky DJ, Oz MC, Koga S, et al. Cardiac preservation is enhanced in a heterotopic rat transplant model by supplementing the nitric oxide pathway. J Clin Invest, 1994, 93:2291-2297.
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