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高压氧通过减轻多器官功能障碍和脑氧化应激来提高中暑大鼠的存活率。

Hyperbaric oxygen improves survival in heatstroke rats by reducing multiorgan dysfunction and brain oxidative stress.

作者信息

Niu Kou-Chi, Lin Mao-Tsun, Chang Ching-Ping

机构信息

Institute of Undersea and Hyperbaric Oxygen Medicine, National Defense Medical Center, Taipei, 116 Taiwan.

出版信息

Eur J Pharmacol. 2007 Aug 13;569(1-2):94-102. doi: 10.1016/j.ejphar.2007.04.037. Epub 2007 Apr 30.

Abstract

Hyperbaric oxygen has been found to be beneficial in treating heatstroke animals. We attempted to further assess the possible mechanism of therapeutic protection offered by hyperbaric oxygen in experimental heatstroke. Anesthetized rats, immediately after the onset of heatstroke, were randomized into the following groups and given: a) hyperbaric oxygen (100% O(2) at 253 kPa for 1 h); or b) normal air. They were exposed to 43 degrees C temperature to induce heatstroke. When the untreated rats underwent heat stress, their survival time values were found to be 20-24 min. Resuscitation with hyperbaric oxygen increased the survival time to new values of 152-176 min. All untreated heatstroke rats displayed cerebrovascular dysfunction (evidenced by hypotension, intracranial hypertension, and cerebral hypoperfusion, hypoxia, and ischemia), hypercoagulable state (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer, but decreased values of platelet count and protein C in plasma), and tissue ischemia/injury (evidenced by increased levels of creatinine, serum urea nitrogen, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase in plasma, and dihydrobenzoic acid, lipid peroxidation, and oxidized-form glutathione/reduced-form of glutathione ratio in hypothalamus). The cerebrovascular dysfunctions, hypercoagulable state, tissue ischemia/injury, and brain oxidative stress that occurred during heatstroke were all suppressed by hyperbaric oxygen therapy. The current results indicate that hyperbaric oxygen therapy may resuscitate rats that had a heatstroke by decreasing multiple organ dysfunction and brain oxidative stress.

摘要

已发现高压氧对治疗中暑动物有益。我们试图进一步评估高压氧在实验性中暑中提供治疗保护的可能机制。麻醉大鼠在中暑发作后立即被随机分为以下几组并给予相应处理:a)高压氧(253 kPa下100%氧气,持续1小时);或b)正常空气。将它们暴露于43摄氏度温度下以诱导中暑。未处理的大鼠遭受热应激时,其存活时间为20 - 24分钟。用高压氧复苏可将存活时间延长至152 - 176分钟的新值。所有未处理的中暑大鼠均表现出脑血管功能障碍(表现为低血压、颅内高压、脑灌注不足、缺氧和缺血)、高凝状态(表现为活化部分凝血活酶时间、凝血酶原时间和D - 二聚体水平升高,但血浆中血小板计数和蛋白C值降低)以及组织缺血/损伤(表现为血浆中肌酐、血清尿素氮、天冬氨酸转氨酶、丙氨酸转氨酶和碱性磷酸酶水平升高,以及下丘脑中二氢苯甲酸、脂质过氧化和氧化型谷胱甘肽/还原型谷胱甘肽比值升高)。中暑期间发生的脑血管功能障碍、高凝状态、组织缺血/损伤和脑氧化应激均被高压氧治疗所抑制。目前的结果表明,高压氧治疗可能通过减少多器官功能障碍和脑氧化应激来使中暑大鼠复苏。

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