Solovyeva E Yu, Karneev A N, Chekanov A V, Baranova O A, Choi I V
Pirogov Russian National Research Medical University, Moscow, Russia.
Zh Nevrol Psikhiatr Im S S Korsakova. 2017;117(5):103-108. doi: 10.17116/jnevro201711751103-108.
Developing brain ischemia due to cerebral vascularization leads to disruption of brain metabolism. Chronic cerebral hypoperfusion leads to irreversible brain damage and plays an important role in the development of some types of dementia. Early use of antioxidants such as ethyl ether apovincamine acid (vinpocetine) and 2-ethyl-6-methyl-3-hydroxypyridine-succinate in the treatment of this pathology is seen as a real pathogenetically based method of correction of cerebral metabolism with cerebral vascular disorders, demonstrating the increase in cerebral blood flow and also neuroprotective effects. Clinical studies and studies on biological models show that the main mechanisms of action of vinpocetine and 2-ethyl-6-methyl-3-hydroxypyridine-succinate, although have a similar focus, but implementing neuroprotective and nootropic effects via various links in the pathogenesis of ischemic brain damage.
由于脑血管形成导致的脑缺血发展会引起脑代谢紊乱。慢性脑灌注不足会导致不可逆的脑损伤，并在某些类型痴呆的发展中起重要作用。早期使用抗氧化剂，如乙基醚长春胺酸（长春西汀）和2-乙基-6-甲基-3-羟基吡啶琥珀酸盐来治疗这种病理状况，被视为一种基于发病机制的真正方法，用于纠正脑血管疾病引起的脑代谢，显示出脑血流量增加以及神经保护作用。临床研究和生物模型研究表明，长春西汀和2-乙基-6-甲基-3-羟基吡啶琥珀酸盐的主要作用机制虽然有相似的重点，但通过缺血性脑损伤发病机制中的各种环节发挥神经保护和益智作用。
