药物预处理后缺血再灌注损伤大鼠心肌重塑与血管紧张素受体表达

目的 观察用肾素血管紧张素系统(RAS)阻断剂药物预处理后,大鼠心肌缺血再灌注损伤中血管紧张素受体的表达与心肌重塑.方法 148只大鼠随机分成四组:假手术组(Sham组)、对照组、血管紧张素转换酶抑制剂(ACEI)组、血管紧张素受体阻滞剂(ARBs)组.术前对照组给予生理盐水灌胃、ACEI组给予福辛普利5 mg·kg-...

Angiotensin receptor expression and myocardium remodelling in IR rat after ACEI/ARBs pretreatment

Objective To observe the distribution of myocardial and expression of AT2R in IR rat under the antagonist pretreatment of RAS.Methods 148 rats were divided randomly into four groups:Sham group,Control group,ACEI group and ARBs group.The Control group were received placebo,ACEI group were received fosinpril(5 mg·kg-1·d-1) and the ARBs group were received valsartan(10 mg·g-1·d-1) respectively via gavage for 4 weeks before surgery.To make IR model,the thorax of rats was opened,and the LAD(left anterior descending coronary artery) was ligated for the control group,ACEI group and ARBs group.After 30 minutes,the ligature was removed and the treatment was continued to use till the heart was removed.On the 3rd,7th,14th,28th postoperation day,rats were killed for the heart(after hemodynamics).The section was stained by picrosirus red and immunohistochemistry to observe collagen deposition in institution and areas around vessels and dynamic expression of AT.Results Collagen deposition in the myocardial interstitial of Control group increased gradually,and there was significantly difference between the Sham group and the Control group at day 7,14,and 28.However,collagen deposition of ACEI group and ARBs group was significantly decreased compared with the Control group.The distribution of AT1R was dispersed,and it was increased for a short period and decreased slowly after IR.While the distribution of AT2R was localized on the membrane of fibroblast in subendocardial,and part of the myocardial membrane.The expression of AT2R was transient after IR under pretreatment of ACEI and ARB.Its reexpression reached a peak at day 7 in Control grouop,while in ARBs group the peak was earlier and higher than that in the Control group.Conclusion ACEI and ARBs may inhibit cardiovascular remodelling effectively.The reexpression of AT2R was transient after IR.It was partly because of the long-term blockade of AT1R after pretreatment of ARBs.