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为探讨一氧化氮 (NO)在阿霉素 (ADR)心肌病中的病理和生理作用。采用SD大鼠 40只 ,随机分为ADR组、L -精氨酸 (L -Arg)组、L -Arg +ADR组及正常对照组 ,于实验第 2、4、6周末分别采血测血清NO、丙二醛 (MDA)含量。结果 :ADR组血清NO值及MDA值逐渐升高 ,显著大于正常对照组 (P <0 .0 0 0 1)。L -Arg组血清NO值均显著高于正常对照组(P <0 .0 1) ;而MDA值无差异。L -Arg +ADR时 ,可使NO升高 ,但升高值与L -Arg组或ADR组相比 ,差异无显著性 ,血清MDA值虽逐渐升高 ,但仍显著低于ADR组 (P <0 .0 5 )。结论 :①ADR可使大鼠诱生NO和促进氧自由基的释放 ,导致大鼠阿霉素心肌病 ;②给予大鼠L -Arg ,促进内皮源性NO的合成 ,反馈抑制具细胞毒性的诱生型NO合酶 (iNOS) ,发挥其抗氧自由基作用 ,使冠状动脉扩张 ,增加冠脉血流 ,从而保护心肌。
To investigate the pathological and physiological role of nitric oxide (NO) in adriamycin (ADR) cardiomyopathy. Forty Sprague - Dawley rats were randomly divided into ADR group, L - Arg group, L - Arg + ADR group and normal control group. At the end of the 2nd, 4th, and 6th week of the experiment, serum NO , Malondialdehyde (MDA) content. Results: Serum NO and MDA values in ADR group were significantly higher than those in normal control group (P <0.0100). Serum NO levels in L-Arg group were significantly higher than those in normal control group (P <0.01), while there was no difference in MDA value. L-Arg + ADR increased NO, but no significant difference compared with L-Arg group or ADR group (P <0.05). Serum MDA level was still significantly lower than that of ADR group (P <0 .0 5). Conclusion: (1) ADR can induce NO in rats and promote the release of oxygen free radicals, resulting in doxorubicin cardiomyopathy in rats; (2) L-Arg is administered to rats to promote the synthesis of endogenous NO and feedback inhibition of cytotoxicity Bioactive NO synthase (iNOS), which exerts its antioxidant free radical action, expands coronary arteries and increases coronary blood flow, thereby protecting the myocardium.