Chumburidze V B
Farmakol Toksikol. 1976 Jan-Feb;39(1):46-50.
Experimental data on the mechanism accounting for the action of a new antianginal drug nonachlazine are presented. Nonachlazine was found to intensively (120+/-9.5 per cent) and protractedly (30--40 min) augment the blood flow in the coronary vessels, increasing the oxygen reserve of the myocardium. The contractile function of the heart and beat ejection considerably gain in their intensity, after an initial short-lived fall (by an average of 26.5+/-3.4 per cent), with the resistance of the coronary vessels declining (21+/-1.0 per cent). Administration of nonachlazine made against the background of a propranol (0.5 mg/kg) block of the beta-adrenergic structures of that by practolol (5 mg/kg) is not accompanied by the above effects. The prevalent influence of nonachlazine on the blood circulation and the function of the heart muscle may be explained by its action on the extravascular factors of the venous blood flow regulation (changes in the metabolism activity of the heart, caused by the stimulation of the beta-adrenergic structures of the myocardium).
本文介绍了关于新型抗心绞痛药物诺那氯嗪作用机制的实验数据。研究发现,诺那氯嗪能强烈(增加120±9.5%)且持久(30 - 40分钟)地增加冠状血管的血流量,提高心肌的氧储备。心脏的收缩功能和射血强度在最初短暂下降(平均下降26.5±3.4%)后显著增强,同时冠状血管阻力下降(21±1.0%)。在普萘洛尔(0.5毫克/千克)阻断β - 肾上腺素能结构或醋氨心安(5毫克/千克)的背景下给予诺那氯嗪,不会出现上述效果。诺那氯嗪对血液循环和心肌功能的显著影响可能是由于其对静脉血流调节的血管外因素起作用(由心肌β - 肾上腺素能结构的刺激引起心脏代谢活动的变化)。