The effect of an angiotensin converting enzyme inhibitor (ACEI) on right ventricular remodeling

在本研究中，我们制备了一种常见于犬的PS模型，并研究了ACEI对心肌重塑的抑制作用。ACEI给药后，通过监测临床状况和各种实验室检查参数，以及通过测量心肌、纤维组织和心肌细胞直径中的酶活性来检查效果。在这个为期60天的实验中，实验室检查显示ACEI组肺动脉流速随时间推移而降低。然而，未观察到ACEI给药引起的临床状况恶化。ACEI组中肺动脉流速降低的原因尚不清楚，因此认为有必要通过进行长期观察来确定这种降低的影响。虽然ACEI抑制了循环血中的ACE活性，但对右心室肌中的ACE活性无明显抑制作用。此外，组织学检查显示PS和ACEI组的右心室壁厚度增加，纤维组织增加，心肌细胞直径增加。因此，未观察到ACEI对心肌重塑的抑制作用。有人认为，这是因为更多的ANG II是由糜蛋白酶比ACE在狗。事实上，在假手术组中，右心室的糜酶活性大于ACE活性。认为将来有必要研究ANG II受体阻滞剂对PS的有用性，其可以控制涉及糜酶的ANG II形成。

In this study, we prepared a PS model that is commonly found in dogs, and examined the inhibitory effect of ACEI on myocardial remodeling. The effect was examined following administration of ACEI by monitoring clinical conditions and various laboratory test parameters, as well as by measuring enzyme activity in cardiac muscle, fibrous tissue and cardiomyocyte diameter.In this 60-day experiment, laboratory tests revealed a time-dependent decrease in flow rate in the pulmonary artery in the ACEI group. However, exacerbation of the clinical conditions caused by administration of ACEI was not observed. The cause of the decrease in flow rate in the pulmonary artery in the ACEI group is unknown, and it is therefore considered necessary to determine the influence of this decrease by carrying out long-term observation. Although ACEI inhibited ACE activity in circulating blood, no significant inhibition of ACE activity was observed in the right ventricular muscle. In addition, histological examinations revealed an increase in the thickness of the right ventricular wall, an increase in fibrous tissue and an increase in cardiomyocyte diameter in both the PS and ACEI groups. As such, inhibition of myocardial remodeling by ACEI was not observed. It was suggested that this is because more ANG II is produced by chymase than by ACE in dogs. In fact, in the Sham group, chymase activity was greater than ACE activity in the right ventricle. It is considered necessary in the future to examine the usefulness of ANG II receptor blockers against PS, which can control ANG II formation that involves chymase.