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机构地区:[1]河北省医学科学院病理生理研究室
出 处:《生理学报》1995年第3期231-237,共7页Acta Physiologica Sinica
摘 要:血管内皮产生的内皮衍生舒张因子(endothelium-derivedrelaxingfactor,EDRF)即一氧化氮(nitricoxide,NO)。本工作分别在大鼠Langendorff离体心脏灌流模型和培养的大鼠心肌细胞上观察了NO、NO的前体物质L-精氨酸(L-Arg)、NO的合成阻断剂L-硝基精氨酸(L-NNA)对心肌缺血(缺氧)再灌注(复氧)损伤的影响。结果:(1)离体心脏停灌30min后,用含NO的K-H液再灌流时可显著增加冠脉流量、左室内压及±dp/dtmax,而用含L-NNA的K-H液再灌流则作用相反。L-Arg可部分逆转L-NNA的收缩冠脉作用,而其单独作用却不能改善心肌血供和心肌收缩力。NO降低心肌组织MDA(丙二醛)和NAG酶(N-乙酰-β-D-氨基葡萄糖苷酶)含量,而L-NNA则使之增加。(2)培养心肌细胞缺氧后复氧,同时加入NO,L-Arg或L-NNA三种物质对心肌细胞内Ca2+含量均无显著影响,但均可降低缺氧再给氧培养液中MDA,NAG酶含量。以上结果表明,NO对缺血(缺氧)、再灌注(复氧)心肌具保护作用。其作用机制可能与NO改善再灌流心肌血供及减弱氧自由基损伤有关。The present study is undertaken to investigate the effects of NO, its inhibitor L-NNA and its procursor L-Arg on the status of myocardial tissue during ischemia (hypoxia ) and reper reperfusion (reoxygenation) in two different models, i. e. Langendorff heart and cultured heart cells of rat. The results were as follows: (1) When heart perfusion was stopped for 30 min and reinstitued for 20 min with K-H buffer containing NO, the coronary flow rate (CFR), left ventricular pressure (LVP) and ±dp/dtmax increased significantly. When NO was replaced by L-NNA opposite effects were observed. L-Arg alone was without effect on CFR, LVP and ±dp/dtmax, but attenuated the decreasing effect of L-NNA on CFR. NO decreased MDA and NAGase content of myocardium while L-NNA increased them. (2) When cultured ventricular myocytes were subjected to hypoxia for 30 min and reoxygenated for 20 min, none of the substances under investigation showed any effects on Ca2+ content of heart cells, but all of them decreased MDA, NAGase content of the cultllre tissue after reoxygendion. The above findinss show thst NO plays an important role in protecting myocardium from ischemic and reperfused injury by improving blood supply of reperfused myocardium and attenuation of oxygen free radical injury.
分 类 号:R541.402[医药卫生—心血管疾病] R363.27[医药卫生—内科学]
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