Simko F, Pechánová O, Bernátová I, Holécyová A, Simko J, Sochorová R
Department of Pathophysiology, Faculty of Medicine, Bratislava, Slovak Republic.
Physiol Res. 1998;47(2):103-7.
The effect of the angiotensin converting enzyme (ACE) inhibitor, captopril, on proteosynthesis in the aorta, acetylcholine-stimulated aortic relaxation and endothelaemia (circulating endothelial cells) was investigated in rabbits with aortic insufficiency. The animals were studied 28 days after experimental intervention. Cardiac volume overload stimulated proteosynthesis in the aorta as reflected by increased ribonucleic acid (RNA) concentration and [14C] leucine incorporation into proteins of the aorta. Moreover, the number of endothelial cells in the blood was increased. The administration of captopril starting from the second day of the haemodynamic overload, partially prevented the increase both in aortic proteosynthesis and in endothelaemia. Despite these alterations, the relaxing ability of the aorta to acetylcholine was not changed either by the haemodynamic overload or by captopril. We conclude that the increase of proteosynthesis in the aorta and of endothelaemia in the early period of chronic cardiac volume overload in rabbits were partially prevented by chronic captopril treatment. Neither aortic insufficiency nor captopril changed the acetylcholine-induced relaxation of the aorta.
在患有主动脉瓣关闭不全的兔子中，研究了血管紧张素转换酶（ACE）抑制剂卡托普利对主动脉蛋白合成、乙酰胆碱刺激的主动脉舒张以及内皮血症（循环内皮细胞）的影响。在实验干预28天后对动物进行研究。心脏容量超负荷刺激主动脉蛋白合成，表现为核糖核酸（RNA）浓度增加以及[14C]亮氨酸掺入主动脉蛋白中。此外，血液中内皮细胞数量增加。从血流动力学超负荷第二天开始给予卡托普利，部分预防了主动脉蛋白合成和内皮血症的增加。尽管有这些改变，血流动力学超负荷或卡托普利均未改变主动脉对乙酰胆碱的舒张能力。我们得出结论，慢性卡托普利治疗部分预防了兔子慢性心脏容量超负荷早期主动脉蛋白合成增加和内皮血症增加。主动脉瓣关闭不全和卡托普利均未改变乙酰胆碱诱导的主动脉舒张。
