Mechanisms of postischemic injury in skeletal muscle: intervention strategies.

Mechanisms of postischemic injury in skeletal muscle: intervention strategies.
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骨骼肌缺血后损伤的机制:干预策略。

DOI:
10.1152/jappl.1996.80.2.369
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发表时间:
1996
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Korthuis,RJ
Korthuis,RJ
中科院分区:
--
文献类型:
--
作者:
Rubin,BB;Romaschin,A;Walker,PM;Gute,DC;Korthuis,RJ

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缺血骨骼肌的再灌注导致不良的局部和全身效应。这些有害作用可以通过干扰或调节在缺血和/或再灌注期间启动的病理生理过程来减弱。本文就骨骼肌缺血再灌注损伤的不同干预策略进行综述,旨在阐明骨骼肌缺血再灌注损伤的发病机制。这些研究的结果表明,导致细胞功能障碍和死亡的缺血后损伤过程本质上是多因素的,包括氧化剂生成、促炎介质的产生、白细胞浸润、Ca 2+过载、磷脂过氧化和消耗、一氧化氮代谢受损和ATP产生减少。虽然骨骼肌缺血-再灌注的发病机制是复杂的,仔细描绘的机制,有助于缺血后微血管功能障碍和肌肉坏死已经发展到合理的干预策略,可能会提出和实施作为潜在的治疗与缺血-再灌注相关的骨骼肌功能障碍。
Reperfusion of ischemic skeletal muscle leads to adverse local and systemic effects. These detrimental effects may be attenuated by interfering with or modulating the pathophysiological processes that are set in motion during ischemia and/or reperfusion. The purpose of this paper is to review the different intervention strategies that have been employed in an attempt to elucidate the mechanisms involved in the pathogenesis of skeletal muscle ischemia-reperfusion injury. The results of these studies indicate that the postischemic injury processes that lead to cell dysfunction and death are multifactorial in nature and include oxidant generation, elaboration of proinflammatory mediators, infiltration of leukocytes, Ca2+ overload, phospholipid peroxidation and depletion, impaired nitric oxide metabolism, and reduced ATP production. Although the etiopathogenesis of skeletal muscle ischemia-reperfusion is complex, careful delineation of the mechanisms that contribute to postischemic microvascular dysfunction and muscle necrosis has progressed to the point where rational intervention strategies may be proposed and implemented as potential treatments for skeletal muscle dysfunction associated with ischemia-reperfusion.
内皮细胞的细胞骨架调节体内血管外多形核白细胞的积累。
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