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作 者:郭宝石[1] 刘洪涛[2] 窦兰君[2] 王静[2]
机构地区:[1]二炮防疫队,北京100071 [2]军事医学科学院卫生学环境医学研究所,天津300050
出 处:《中国应用生理学杂志》2001年第4期370-372,共3页Chinese Journal of Applied Physiology
摘 要:目的 :观察一氧化氮 (NO)对相对缺血再灌注心肌损伤的保护作用。方法 :高频弱电流刺激法建立离体心肌相对缺血再灌注模型 ,设非缺血组和相对缺血组 ,相对缺血组包括对照、L 精氨酸 (L ARG)、硝基 L 精氨酸甲酯 (L NAME)三组。测定缺血前和再灌注时心功能变化、NO含量和乳酸脱氢酶同功酶 1(LD 1)活性。结果 :L ARG可明显促进再灌注期间NO合成 ,抑制LD 1活性升高。再灌注 40min时 ,L ARG组心肌功能恢复程度明显高于对照组和L NAME组 (P <0 .0 5 ) ,L NAME使心肌NO含量降低 (P <0 .0 5 ) ,LD 1活性升高 (P <0 .0 5 ) ,心功能恢复程度最低。结论 :NO可明显减轻心肌缺血再灌注时的细胞损伤 。Aim: The protective effect of L arginine on relative ischemia/reperfusion induced myocardial injury was investigated in the rat isolated langendoff perfused heart. Methods: Four groups of hearts subjected to 20 min electric stimulus and 40 min reperfusion received vehicle,L arginine,N ω nitro L arginine methyl ester and only stimulus respectively. Results:The recovery of left ventricular developed pressure and pressure rate product at the end of reperfusion was significantly higher in the L arginine group (89.04%±2.46% and 72.16%±4.40%,respectively) than in the vehicle group(64.74%±7.67% and 44.57%±6.89%,respectively, P <0.05). It is suggested that N ω nitro L arginine methyl ester inhibits the recovery of the heart function after ischemia and accelerates the myocardial injury. Conclusion: We propose that it is important to protect the integrity of the heart angioendothelium during ischemia/reperfusion,and promote the synthesis of NO to relieve the myocardial injury and consequently accelerate the recovery of the heart function.
关 键 词:心肌缺血 再灌注损伤 一氧化氮 乳酸脱氢酶同功酶-1
分 类 号:R542.2[医药卫生—心血管疾病]
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