首页> 外文期刊>American Journal of Physiology >Differential response to myocardial reperfusion injury in eNOS-deficient mice.
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Differential response to myocardial reperfusion injury in eNOS-deficient mice.

机译:eNOS缺陷小鼠对心肌再灌注损伤的差异反应。

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Two strains of endothelial nitric oxide synthase (eNOS)-deficient (-/-) mice have been developed that respond differently to myocardial ischemia-reperfusion (MI/R). We evaluated both strains of eNOS(-/-) mice in an in vivo model of MI/R. Harvard (Har) eNOS(-/-) mice (n = 12) experienced an 84% increase in myocardial necrosis compared with wild-type controls (P < 0.05). University of North Carolina (UNC) eNOS(-/-) (n = 10) exhibited a 52% reduction in myocardial injury versus wild-type controls (P < 0.05). PCR analysis of myocardial inducible NO synthase (iNOS) mRNA levels revealed a significant (P < 0.05) increase in the UNC eNOS(-/-) mice compared with wild-type mice, and there was no significant difference between the Har eNOS(-/-) and wild-type mice. UNC eNOS(-/-) mice treated with an iNOS inhibitor (1400W) exacerbated the extent of myocardial necrosis. When treated with 1400W, Har eNOS(-/-) did not exhibit a significant increase in myocardial necrosis. These data demonstrate that two distinct strains of eNOS(-/-) mice display opposite responses to MI/R. Although the protection seen in the UNC eNOS(-/-) mouse may result from compensatory increases in iNOS, other genes may be involved.
机译:已开发出两种内皮一氧化氮合酶(eNOS)缺陷(-/-)小鼠品系,它们对心肌缺血再灌注(MI / R)的反应不同。我们在MI / R的体内模型中评估了eNOS(-/-)小鼠的两种菌株。与野生型对照组相比,哈佛(Har)eNOS(-/-)小鼠(n = 12)的心肌坏死增加了84%(P <0.05)。北卡罗来纳大学(UNC)的eNOS(-/-)(n = 10)与野生型对照组相比,心肌损伤降低了52%(P <0.05)。心肌诱导型NO合酶(iNOS)mRNA水平的PCR分析显示,与野生型小鼠相比,UNC eNOS(-/-)小鼠明显增加(P <0.05),而Har eNOS(- /-)和野生型小鼠。使用iNOS抑制剂(1400W)处理的UNC eNOS(-/-)小鼠加剧了心肌坏死的程度。当用1400W处理时,Har eNOS(-/-)并未显示出心肌坏死的明显增加。这些数据表明,两个不同的eNOS(-/-)小鼠品系显示出对MI / R的相反反应。尽管在UNC eNOS(-/-)小鼠中看到的保护作用可能是iNOS的补偿性增加引起的,但其他基因可能也参与其中。

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