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Mechanisms of Endothelial Dysfunction in Pathologies of Various Genesis

机译:各种创世纪病理病理中内皮功能障碍机制

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Studies in the experiment and the clinic demonstrated the nature of changes in the system of POL - AOC, nitric oxide homeostasis and cholesterol as factors contributing to dysfunction of the vascular endothelium. In metabolic syndrome in pregnant women and in patients with myocardial ischemia, as well as in intoxication syndrome (cobalt chloride), the induction of the lipid peroxidation process according to malonic aldehyde and impaired AODS cells was detected. A deficit of nitric oxide (NO), a violation of its bioavailability and vasoconstriction develops. Consequently, lipid peroxidation-triggering factors: elevated blood glucose, impaired oxygen supply to the myocardium (ischemia), and exposure to cobalt chloride play an important role in disrupting the formation of nitric oxide and adaptive mechanisms from reactive oxygen species (ROS). Disruption of nitric oxide homeostasis (eNOS/NO) plays a decisive role in the genesis of vascular complications and can be considered a biochemical marker for the development and progression of various pathologies. Based on these data, it is possible to develop a methodology for correcting the pathogenetic orientation.
机译:实验中的研究和诊所展示了Pol - Aoc,一氧化氮稳态和胆固醇系统的变化的性质,因为有助于血管内皮功能障碍。在,根据丙二醛和受损细胞AODS脂质过氧化过程的诱导在孕妇和在心肌缺血患者代谢综合征,以及在中毒综合征(氯化钴)检测。一氧化氮(NO)的缺陷,违反其生物利用度和血管收缩。因此,脂质过氧化触发因素:升高的血糖,氧气供应到受损心肌(局部缺血),和暴露于氯化钴在破坏一氧化氮和适应机制的活性氧物种(ROS)的形成中发挥重要作用。一氧化氮稳态(Enos / No)的破坏在血管并发症的成因中起着决定性作用,并且可以被认为是各种病理学的发展和进展的生物化学标志。基于这些数据,可以制定用于校正致病的方法。

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