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Mild Therapeutic Hypothermia for Treatment of Cardiac Arrest: Current Results and Future Perspectives

机译:用于治疗心脏骤停的轻度治疗性低温:当前结果和未来的观点

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Sudden cardiac arrest remains a major unresolved public health problem. It is still the leading cause of death, and few cardiopulmonary-cerebral resuscitation (CPCR) attempts on cardiac arrest victims result in neurologically intact long-term survivors [1,2].The pathogenesis of cerebral ischemia and post-ischemic encephalopathy are multifactorial and only partially understood [2-5]. Brain ischemia results in rapid loss of high-energy phosphate compounds [6] and generalized membrane depolarization with an increase in intracellular calcium and the release of large amounts of glutamate [4]. These mechanisms initiate multiple independent chemical cascades and fatal pathways during reperfusion, resulting in neuronal death due to necrosis and apoptosis [5]. Due to the multifactorial pathogenesis of post-arrest neuronal death, multifaceted treatment strategies or a combination of single-molecule targeted drugs is required to achieve survival without brain damage [7,8].
机译:突然的心脏骤停仍然是一个主要的未解决的公共卫生问题。它仍然是死亡的主要原因,很少有心肺脑复苏(CPCR)对心脏抑制受害者的尝试导致神经学完整的长期幸存者[1,2]。脑缺血和缺血后脑病的发病机制是多因素和缺血性脑病仅部分理解[2-5]。脑缺血导致高能磷酸盐化合物[6]和广义膜去极化的快速丧失,随着细胞内钙的增加和大量谷氨酸的释放[4]。这些机制在再灌注过程中发起多种独立的化学级联和致命途径,导致由于坏死和细胞凋亡导致神经元死亡[5]。由于捕获后神经元死亡的多因素发病机制,多方刻录的治疗策略或单分子靶向药物的组合需要在没有脑损伤的情况下达到存活[7,8]。

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