摘要
目的旨在探讨内皮细胞损伤、功能改变在心肌缺血再灌注（ＭＩＲ）损伤中的发病机制及其与心肌梗塞面积的关系及卡托普利的保护作用。方法用２４只麻醉兔随机分为三组，（１）ＭＩＲ组，（２）ＭＩＲ＋卡托普利治疗组，（３）假手术对照组，观察心肌缺血半小时，再灌注０．５、１．５、６小时血循环内皮细胞（ＣＥＣ），一氧化氮（ＮＯ），内皮素（ＥＴ）的含量变化及其与心肌梗塞面积的关系，静注卡托普利观察其对梗塞面积及上述指标的影响。结果（１）与假手术组比较，再灌注半小时，血ＮＯ下降，ＥＴ升高，其变化于再灌注６小时最明显（Ｐ＜０．０５），ＣＥＣ则以再灌注１．５小时明显增高（Ｐ＜０．０５）；（２）再灌注６小时心肌梗塞范围较治疗组明显增加（Ｐ＜０．０５），且同一时相点血ＮＯ与心肌梗塞面积呈负相关（ｒ＝－０．９６１，Ｐ＜０．０１），血ＥＴ与心肌梗塞面积呈正相关（ｒ＝０．９２３，Ｐ＜０．０５）；（３）用卡托普利干预后，血ＮＯ有所回升，ＥＴ明显下降，心肌梗塞面积明显缩小。结论ＭＩＲ可诱发内皮功能紊乱。
Objective To study the damage and functional changes of endothelial cells (EC) and their relation to the extent of myocardial infarction in myocardial ischemia reperfusion(MI/R) and the therapeutic effect of captopril. Methods 24 rabbits were ramdomized into 3 groups ( n =8 in each):MI/R group (A), Captopril group (B) and sham operated group(c). Plasma Endochelin (ET), ntric oxide (NO), circulation endothelial cells (CEC) were measured before ligation of the coronary artery, 0.5 hour after ischemia and 0.5, 1.5 and 6 hours after reperfusion. Area of myocardial infarction was measured at the last time point in both MI/R and Captopril group. Results (1) Comparing with group C,NO decreased and ET increased in 0.5h ( P <0.05)and more significantly in 1.5 h and 6h after reperfusion ( P <0.01). The number of CEC increased 1.5 h after reperfusion ( P <0.01); (2)ET was positively correlated with the area of MI ( r =0.923, P <0.05);NO was negatively correlated with the area of MI( r =-0.961, P <0.01); (3)Captopril improved the change of biochemical indices mentioned and reduced the area of MI.Conclusions Reperfusion results in dysfunction of endothelium as indica ted by NO decrease,and ET increase and endothelium dysfunction my initiate myocardial injury.
出处
《中华内科杂志》
CAS
CSCD
北大核心
1998年第11期736-738,共3页
Chinese Journal of Internal Medicine
