摘要
目的 测定心肌缺血再灌注过程中不同时点一氧化氮合酶 (nitrieoxidesynthase ,NOS)活性、基因表达水平及一氧化氮 (nitricoxide,NO)产量。方法 结扎新西兰白兔冠状动脉左前降支建立在体心肌缺血再灌注模型。测定正常、缺血 3 0min、 60min、缺血 60min再灌注 3 0min、 60min、 12 0min心肌NOS活性、内皮性一氧化氮合酶 (endothelialnitricoxidesynthase,eNOS)、诱生性一氧化氮合酶 (induciblenitricoxidesynthase ,iNOS)基因表达水平及NO产量。结果 正常心肌和缺血 60min再灌注 12 0min心肌NOS活性高于缺血心肌 ,(P <0 0 1)。正常心肌和缺血 60min再灌注 12 0min心肌NO含量、eNOS基因表达水平高于其余各时点心肌 (P<0 0 5 )。各时点心肌均未见到iNOS基因的表达。结论 ( 1)在缺血期及再灌注的初期 (≤ 1小时 ) ,心肌eNOS活性 ,基因表达水平及NO含量均明显降低。 ( 2 )至恢复灌注 2小时 ,心肌eNOS活性、基因表达水平及NO含量均已接近基础水平。 ( 3 )缺血 1小时 ,恢复灌注 2小时并无iNOS活性或基因表达。
Objective To determine the dynamic changes of the activity of nitrogen monoxide synthase (NMS), the level of gene expression and the output of nitrogen monoxide during myocardial ischemia and refilling. Methods The animal model of New Zealand rabbit was made by ligating left anterior descending branch of coronary artery. The activity of NMS, the level of gene expression of endothelial NMS and induced NMS and the output of nitrogen monoxide in myocardium were determined in normal status, ischemia for 30min and 60min, and refilling for 30min, 60min and 120min. Results The activity of NMS, the level of gene expression of endothelial NMS and the output of nitrogen monoxide in normal status and refilling for 120min were significantly higher than others. But the level of gene expression of induced NMS wasn't detected anytime in the experiment. Conclusions (1) The activity of NMS, the level of gene expression of endothelial NMS and the output of nitrogen monoxide are significantly decreased during myocardial ischemia and early phase of refilling(≤60min). (2) The above items approaches to the basal level after refilling for two hours. (3) During the whole course of experiment, there is no expression of induced NMS.
出处
《浙江预防医学》
2003年第6期10-11,15,共3页
Zhejiang Journal of Preventive Medicine
基金
浙江省科技厅资助 (编号 0 0 1110 2 34)
关键词
一氧化氮合酶
心肌缺血再灌注损伤
基因表达
测定
兔
Nitrogen monoxide synthase(NMS) Nitrogen monoxide Myocardial ischemia and refilling