精氨酸加压素受体拮抗剂在实验性充血性心力衰竭力的作用

目的：探讨精氨酸加压素受体拮抗剂在慢性充血性心力衰竭中的作用。方法：大鼠左冠拮扎，造成左室大面积梗死，存活10周，行左心室，股动脉，。股静脉插管，测定其收缩压（SBP），舒适压（DBP），平均动脉后（MBP），左心室压峰值（LVSP），左室舒张末期压（LVEDP），左室内压最大上升速率（＋d/dtmax)，左室内压最大下降速率（－dp/dtmax)，收缩期心力环L（1＋2），舒张期心力不环（L（3＋4），总心力环（Lo)及心率HR，LVEDP＞2kPa大鼠随机分为：（1）心衰给精氨酸加压素（AVP）V1／V2受体拮抗剂组；（2）心衰给50g/L葡萄糖（GS）组，另设（3）假手术组，静注V1／V2受体拮抗剂，3组产测定给药前及给药后10，20，30，40，60，90，120min时间点血液动力学及心肌舒缩下降，并持续到实验结束，30min时＋dp/dtmax及－dp/dtmaxz增加，并于40min时升至最大，伴有L（1＋2），L（3＋4）和L0的明显增加，结论，心衰大鼠静注AVP V1／V2受体拮抗剂后，心肌的收缩，舒张功能得以改善，对充血性心衰有一定的治疗作用。

Role of argininevasopressin receptor antagonist in experimental congestive heart failure

AIM:To investigate the role of arginine vasopressin (AVP) receptor antagonist in chronic congestive heart failure. METHODS:The left coronary artery was ligated to produce a large infarct on the left ventricle,and the rat survived for 10 weeks. Left ventricle,arteria femoralis and femoral vein were cannulated to measure the SBP,DBP,MBP,LVSP,LVEDP,+dp/dtmax,-dp/dtmax,L(1+2),L(3+4),Lo and HR. The rats with LVEDP >2 kPa were randomly divided into 2 groups:①The group of rats with heart failure received AVP V1/V2 receptor antagonist;②The group of rats with heart faulure received 50 g/L GS. ③ A group of sham-operated rats was given,which received V1/V2 receptor antagonist. Parameters of hemodynamics and cardiac systolic,diastolic functions were recorded before and 10,20,30,40,60,90 120 min after infusion in the three groups. RESULTS:There was no change in SBP,DBP,MBP， LVSP and HR in rats with heart failure after infusion of AVP receptor antagonist. 20 min after antagonist infusion,the LVEDP of the rats with heart failure decreased significantly,which lasted to the end of the experiment. 30 min after antagonist infusion,+dp/dtmax and -dp/dtmax increaesed obviously and reached the peak 40 min after the infusion. And at the same time L(1+2),L(3+4) and Lo increased significantly. CONCLUSION:After infusion of AVP V1/V2 receptor antagonist in rats with heart faulure cardiac systolic, diastolic function were improved,which has therapeutic effect on congestive heart failure.