一氧化氮与一氧化氮合酶对心肌的保护作用  

The protection effect of nitric oxide and nitric oxide synthas to myocardium

作　　者：董嘉良[1] 康少平[2] 康英姿[1] 于公元[1] 张艳君[1] 

机构地区：[1]天津医科大学生物化学教研室,天津300070 [2]河北北方学院

出　　处：《天津医科大学学报》2010年第3期429-432,436,共5页Journal of Tianjin Medical University

摘　　要：目的:测定心肌缺血再灌注与心肌缺血后处理时大鼠心肌损伤程度,探讨一氧化氮(NO)与一氧化氮合酶(NOS)对心肌的保护作用。方法:将健康雄性Wistar大鼠分为对照组、实验组、激动剂组及抑制剂组4组,建立离体心肌缺血再灌注损伤模型。使用高效液相色谱仪(HPLC)测定心脏灌流液中NO的含量与心肌中NOS活性。测定乳酸脱氢酶(LDH)活性及心肌梗死面积。结果:平衡末,4组之间冠状动脉循环液中NO含量差异无统计学意义(P>0.05);对照组处理后与实验组后处理后NO含量相比差异有统计学意义(P<0.05);激动剂组再灌注后与对照组处理后NO含量相比差异有统计学意义(P<0.05);抑制剂组后处理后与实验组后处理后NO含量相比差异有统计学意义(P<0.05)。实验组心肌组织NOS活性高于激动剂组与抑制剂组(P<0.05)。实验组心肌组织LDH活性低于激动剂组与抑制剂组(P<0.05)。实验组与对照组梗死面积比较差异有统计学意义(P<0.05);激动剂组及抑制剂组心肌梗死面积均低于对照组(P<0.05)。结论:NO可有效降低缺血再灌注对心肌的损伤。NO与NOS在缺血后处理对再灌注损伤心肌保护机制中起重要作用。Objective： To approach protection effect of nitric oxide （NO） and nitric oxide synthas （NOS） to myocardium. Methods： Healthy Wistar rats were divided into four groups： control group, experiment group, excitomotory group and inhibitory group. Ischemia-reperfusion injury isolated heart model was established.NO content in the perfusion fluid and the activity of NOS in the myocardium were measured by high-performance liquid chromatography （HPLC） directly. The LDH activity and the myocardial infarct size were determined. Results： There was no statistic differences on the NO content among the four groups at the end of equilibrium （P〉0.05）. NO content after reperfusion in the experiment group was significantly higher than that after postconditioning in the control group（P〈0.05）. There was statistic differences between the control group and the excitomotory group on the NO content at the end of equilibrium （P〉0.05）. NO content after postconditioning in the experiment group was significantly higher than that after reperfusion in the inhibitory group （P〈0.05）. Activity of NOS in the experiment group was significantly higher than that in the excitomotory group and the inhibitory group. The LDH activity in both the excitomotory group and the inhibitory group were higher than that in the experiment group. Infarct size in the experiment group attenuated significantly than that in the control group （P〈0.05）. Infarct size in the excitomotory group and the inhibitory group were significantly smaller than that in the control group（P〈0.05）. Conclusion： NO can degrade myocardial damage caused by ischemia-reperfusion efficiently.

关 键 词：缺血再灌注 缺血后处理 一氧化氮 一氧化氮合酶 高效液相色谱 大鼠 

分 类 号：R542.22[医药卫生—心血管疾病]