卡维地洛对急性心肌梗死大鼠血流动力学和心肌胶原含量的影响

目的研究卡维地洛(Carvedilol)对大鼠急性心肌梗死(AMI)后血流动力学的影响及其与心肌组织中胶原含量的关系。方法23只AMI术后存活的雄性SD大鼠随机分为AMI对照组(n=11)和卡维地洛治疗(Carvedilol)组(n=12),另设假手术组(n=11)。给药6周后测量室间隔超声背向散射参数(平均背向散射积分标化值IBS%,背向散射积分周期变化值CVIB)及血流动力学参数、心功能指标。结果(1)与假手术组相比,AMI组大鼠SBP、DBP、LVSP及±dp/dtmax及其校正值(±dp/dtmax/LVSP)均显著降低,LVEDP显著增高,高频超声检测显示IBS%显著升高,CVIB显著降低(均为P<0.05)。(2)与AMI组相比,Carvedilol治疗组大鼠SBP、DBP及LVSP均未进一步降低(P>0.05),LVEDP显著降低,±dp/dtmax及其校正值(±dp/dtmax/LVSP)显著升高,高频超声检测显示IBS%显著降低,CVIB显著升高(均P<0.05)。结论第3代β受体阻滞剂Carvedilol的干预有助于恢复AMI大鼠受损的左室功能,这可能与其抑制非梗死区心肌胶原过度沉积有关。

Effects of carvedilol on hemodynamics and myocardial collagen content after acute myocardial infarction in rats

Objective To investigate the effects of carvedilol on hemodynamics and myocardial collagen content after acute myocardial infarction(AMI)in rats. Methods Twenty-four hours after ligating left anterior descending coronary artery, 23 surviving AMI male Sprague-Dawley rats were randomly assigned to AMI control(n=11),and carvedilol(n=12, 1 mg·kg-1·d-1)group.Eleven rats without coronary artery ligation was taken as sham operation group. After 6 weeks of administration of the drug by gastric gavage, ultrasonic integrated backscatter parameters, hemodynamics and left ventricular function were measured by echocardiography. Results (1)Compared with the sham operation group, hemodynamics in AMI group were deteriorated. SBP,DBP,left ventricular systolic pressure(LVSP) and ±dp/dtmax were significantly decreased,while LVEDP was markedly increased in AMI rats. High-frequency ultrasound detecting showed that integrated backscatter(IBS%) was increased and cyclic variation of integrated backscatter(CVIB) was decreased significantly in AMI rats. (2)There was no statistical difference in SBP,DBP and LVSP between AMI control group and carvedilol group. Compared with the AMI group,carvedilol group had significantly decreased IBS% and LVEDP,and significantly increased CVIB and ±dp/dtmax. Conclusions Carvedilol may effectively improve hemodynamics and left ventricular function after AMI in rats by reducing the collagen deposition in noninfarcted area of left ventricle.