摘要
目的探讨一氧化氮(NO)在大鼠心肌缺血/再灌注损伤(IRI)中的作用。方法20只Wistar雄性大鼠随机分成假手术组,缺血30min再灌注180min组(IRI组)。检测:①心肌组织及血清中NO2-+NO3-值;②心功能指标:心率(HR)和平均动脉压(MAP);③血清肌酸激酶同工酶(CK-MB)含量;④以缺口末端标记法(TUNEL)检测心肌细胞凋亡的变化。结果心肌细胞缺血再灌注后:①心肌组织NO2-+NO3-IRI组较假手术组增高26.7%(P<0.05),血清NO2-+NO3-IRI组较实验后较实验前升高41.1%(P<0.01);②HR和MAPIRI组显著低于假手术组;③血清CK-MB含量IRI组较假手术组升高51%(P<0.01);④心肌组织TUNEL染色IRI组检测到大量阳性凋亡细胞,凋亡细胞阳性指数(AI)IRI组较假手术组升高89.4%(P<0.01)。结论NO升高可能是诱导细胞凋亡,加重心肌细胞缺血/再灌注损伤的重要原因之一。
Objective To study the role of nitric oxide （NO） in myocardial ischemia reperfusion injury （IRI） in rat models. Methods Twenty Wistar male rats were randomized into two groups： the Sham-group and IRI group. IRI model was produced by 30-min ischemia and 180-rain reperfusion. Contents of NO^2-＋NO^3- in myocardium homogenate and in serum, serum level of creatine kinase isoenzyme MB （CK-MB） were determined, cardiac functional indices （heart rate [HR] and mean artery pressure [MAP]） were recorded, and cardiomyocyte apoptosis was examined by TUNEL techniques. Results Compared with the Sham group, IRI group showed： （1） increases in myocardial NO2-±NO3- by 26.7% （P〈0.05） and in serum level of NO2-＋NO3- by 41.1% （P〈0.01）; （2） significantly lowered HR and MAP; （3） elevation in the level of CK-MB by 51% （P〈0.01）; （4） a large number of apoptotic cardiomyocytes, leading to a rise in apoptosis index （AI） as much as 89.4% （P〈0.01）. Conclusion The higher level of NO might be one of important factors contributive to induction of myocardial apoptosis and deteriorated progression of IRI.
出处
《中国药物与临床》
CAS
2007年第3期197-199,共3页
Chinese Remedies & Clinics
关键词
心肌
一氧化氮
细胞凋亡
再灌注损伤
Myocardium
Nitric oxide
Apoptosis
Ischemia reperfusion injury
