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肿瘤坏死因子和氧自由基在老龄大鼠多器官衰竭的变化*范利常润英王士雯金道山余颂涛高宇红(解放军总医院老年心脏科老年医学研究所,北京100853)内毒素血症导致的老年多器官功能衰竭(以下简称MOF)在临床上极为常见。本文通过对内毒素所致的老龄大鼠MOF模... 相似文献
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肾上腺素对幼龄小鼠胸腺褪黑素受体的调节 总被引:3,自引:0,他引:3
应用放射配体结合法检测幼龄小鼠胸腺褪黑素受体(MR),并以此为实验模型研究肾上腺素(E)对胸MR的影响及作用机制。结果表明,生理浓度的E即对胸MR有明显抑制作用,其抑制效应具时间依赖性及剂量依赖性。β-肾上腺素能受体拮抗剂普萘洛尔可逆转引抑制效应,CAMP对MR也有明显抑制作用,表现E对MR的抑制是通过β受体而实现的。这些结果提示,E在生理情况下即对胸腺MR有调节作用。 相似文献
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The role of endothelium-derived relaxing factor (EDRF) on the effect of oxygen-derived free radicals (generated by xanthine-xanthine oxidase system) on intrapulmonary arterial in chronic hypoxic rats was studied by a microbioassay method. Intrapulmonary artery rings with intact or denuded endothelium of hypoxic (5,000 m, 10 days) and normoxic rats were prepared for observation of oxygen-derived free radicals induced contraction. It was shown that oxygen-derived free radicals induced contractions of intrapulmonary arterial rings with intact endothelium were obviously augmented in hypoxic rats than in normoxic controls. The augmented responses could be further potentiated by the addition of EDRF inactivator reduced hemoglobin (RHb), but diminished or even abolished by applying superoxide dismutase (Cu-Zn SOD). However, no effect on denuded rings was observed when RHb or SOD was added. It is concluded that chronic hypoxia may attenuate the action of EDRF in the enhancement of the reactivity of intrapulmonary artery to oxygen-derived free radicals. 相似文献
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通过Bpoc·Ser(tBu)·Asp·OtBu的β-羧基上树脂和依次用Fmoc·Gly·Gly·OHFmoc·Gln·ONP,Fmoc.Ser(tBu).OH,Fmoc.Lys(Boc)·OH,Fmos·Ala·OH及pGlu·OH伸长,接着氨解和酸解的策略,我们用固相方法合成了血清胸腺因子(FTS,Thymulin),pGlu·Ala·Lys·Ser·Gln·Gly·Gly·Ser·Asn;制备了具有最大生物活性的该因子和Zn~(2+)的复合物,FTS-Zn;用该复合物与牛血清白蛋白(BSA)结合所形成的免疫原免疫家兔,获得了抗FTS-Zn~(++)的抗血清,通过酶联免疫吸附分析法(ELISA)测得其滴度高达1:12800。 相似文献
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血管内皮舒张因子在氧自由基所致慢性缺氧大鼠肺内动脉收缩中的作用 总被引:1,自引:0,他引:1
以黄嘌岭(X)-黄嘌呤氧化酶(XO)系统产生氧自由基,应用微量生物测定法观察慢性缺氧(5000m,10d)对大鼠氧自由基所致肺内动脉收缩的影响及内皮舒张因子(EDRF)在其中的作用。慢性缺氧大鼠有内皮的肺内动脉环对氧自由基的收缩反应较正常环境中的对照动物明显增强,加入EDRF灭活剂还原型血红蛋白(RHb)后更加显著;而加入超氧化物歧化酶(铜锌SOD)后则减弱,甚至消除。反之,不论加入RHb或SOD对氧自由基所致去内皮肺内动脉环的收缩反应均无明显影响。上述结果表明慢性缺氧引起肺内动脉收缩增强与EDRF有密切关系:慢性缺氧可能使EDRF的作用减弱,肺内动脉对氧自由基的反应性增强。表示EDRF及其与氧自由基的关系在慢性缺氧性肺动脉高压的形成中可能具有十分重要的意义。 相似文献
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