脑缺氧缺血性损伤患者心脏外科干预阶段糖酵解和细胞生物能量状态的机制

Dmytro Mankovsky
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摘要

目的:研究心脏手术(CS)前后缺氧缺血性脑病变(HIBL)患者人工循环(AC)氧化稳态(OH)生物能量供应的特点。方法和对象。对38例患者进行临床和生化研究,其中缺血性脑卒中14例,脑病15例,重度认知功能障碍9例。结果。通过对CS前后细胞糖酵解活性代谢指标和能量稳态的分析,揭示了糖酵解机制瓦解、厌氧机制强化、细胞能量供应受限的变化规律。所获得的数据证实了CS患者术后特异性代谢提供生物能的形成,考虑到细胞的生物能代谢状态和糖酵解的主导机制,应将其视为HIBL和术前抗氧化脑保护个体化的触发因素之一。结论。术前抗氧化脑保护作为预防人工循环心脏手术中缺氧缺血性脑病变的手段,应以测定生物能量和代谢储备为基础,不应考虑抗氧化药物抑制对其的消耗,因为在线粒体生物能量代谢抑制的同时激活厌氧糖酵解是脑缺血性病变形成或加重的一个因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanisms of glycolysis and bioenergy state of cells at the stages of cardiosurgical interventions in patients with hypoxic — ischemic impairments of the brain
Objective — to study the features of bioenergetic provision of oxidative homeostasis (OH) in patients with hypoxic‑ischemic brain lesions (HIBL) before and after cardiac surgery (CS) using artificial circulation (AC). Methods and subjects. Clinical and biochemical studies were performed in 38 patients, including 14 with ischemic stroke, 15 with encephalopathy, and 9 with severe cognitive dysfunction. Results. Analysis of metabolic indicators of glycolysis activity and energy homeostasis of cells before and after CS revealed the patterns of changes in the disorganization of glycolysis mechanisms, intensification of anaerobic mechanisms while limiting the energy supply of cells. The obtained data confirm the formation of specific postoperative metabolic provision of bioenergy in patients with CS, which should be considered as one of the triggers of HIBL and individualization of antioxidant cerebroprotection in the preoperative period, taking into account the state of bioenergetic metabolism of cells and the dominant mechanisms of glycolysis. Conclusions. Preoperative antioxidant cerebroprotection as a means of prevention of hypoxic‑ischemic brain lesions during cardiac surgery using artificial circulation should be based on the determination of bioenergetic and metabolic reserves, the depletion of which by antioxidant drugs suppression should not be considered, as activation of anaerobic glycolysis at simultaneous metabolic suppression of mitochondrial bioenergetics is a factor of formation or aggravation of ischemic lesions of brain.  
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