Bobkov Iu I, Bobkova V M
Patol Fiziol Eksp Ter. 1991(6):39-41.
The role of altered adrenergic regulation in the development of myocardial pathology was studied in dog experiments. Activation of the sympathetico-adrenal system was induced by electrostimulation of the sympathetic tonic cardiac nerve in the first experimental series and by intravenous infusion of exogenous noradrenaline (NA) in a dose of 1 microgram/kg/min in the second series. A positive inotropic response of the heart occurred in both series. Comparison of the effect of nerve stimulation with the effect of exogenous NA showed them to be essentially different. The NA-mediator secreted in stimulation of the nerve contributed to the development of coronarogenic myocardial ischemia which was confirmed by ECG and the results of study of the coronary blood flow. Infusion of NA from an ampule in the above-mentioned doses failed to produce an effect on the alpha-receptors of the coronary vessels, but by activating the beta 2-receptors of the coronary arteries facilitated their dilatation and thus increased the blood flow in them. The functional relationship between the sympathetic tonic nerve and the alpha-adrenoreceptors of the coronary arteries and between the humoral catecholamines and their beta 2-adrenoreceptors is shown.
在犬类实验中研究了肾上腺素能调节改变在心肌病理发展中的作用。在第一个实验系列中,通过电刺激交感紧张性心脏神经诱导交感-肾上腺系统激活;在第二个系列中,通过以1微克/千克/分钟的剂量静脉输注外源性去甲肾上腺素(NA)来诱导激活。两个系列中均出现了心脏的正性肌力反应。将神经刺激的效果与外源性NA的效果进行比较,发现它们存在本质差异。神经刺激时分泌的NA介质导致了冠状动脉性心肌缺血的发展,这通过心电图和冠状动脉血流研究结果得到证实。以上述剂量从安瓿中输注NA未能对冠状动脉的α受体产生影响,但通过激活冠状动脉的β2受体促进了它们的扩张,从而增加了冠状动脉内的血流。研究显示了交感紧张性神经与冠状动脉α肾上腺素能受体之间以及体液儿茶酚胺与其β2肾上腺素能受体之间的功能关系。