Brain cooling causes attenuation of cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke
Brain cooling causes attenuation of cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke
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DOI：
10.1097/01.shk.0000223124.49265.10
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发表时间：
2006-08-01
期刊：
影响因子：
3.1
通讯作者：
Lin, Mao-Tsun
中科院分区：
文献类型：
--
作者：
Hsu, Shu-Fen;Niu, Ko-Chi;Lin, Mao-Tsun
本研究的目的是评估低温逆行颈静脉冲洗（HRJVF）对中暑的治疗效果。 HRJVF 通过颈外静脉输注 4 摄氏度等渗氯化钠溶液（1.7 mL/100 g 体重，持续 5 分钟）来完成。中暑发生后，立即将麻醉大鼠分为2个主要组并给予以下药物：36℃或4℃等渗氯化钠溶液，静脉注射。他们暴露在43摄氏度的环境温度下导致中暑。另一组大鼠暴露于室温（24℃）并用作常温对照。当WC盐水处理的大鼠经历热暴露时，它们的存活时间值为23至28分钟。中暑发作后立即进行静脉注射复苏。 4摄氏度盐水的剂量显着提高了中暑期间的存活率（208-252分钟）。所有热应激动物均表现出全身炎症和凝血激活，表现为肿瘤坏死因子α、凝血酶原时间、活化部分凝血活酶时间和D-二聚体增加，以及血小板计数和蛋白C减少。生化标记物显示细胞缺血和损伤/功能障碍：血尿素氮、肌酐、谷氨酸草酰乙酸转氨酶、谷氨酸丙酮酸转氨酶和碱性磷酸酶的血浆水平；甘油、谷氨酸和乳酸/丙酮酸的纹状体水平；二羟基苯甲酸、脂质过氧化、氧化型谷胱甘肽、还原型谷胱甘肽、多巴胺和血清素在中暑期间均升高。中暑期间，核心温度和大脑温度以及颅内压也会升高。相比之下，中暑时平均动脉压、脑灌注压、纹状体局部血流水平、氧分压、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性均显着降低。 HRJVF 显着抑制了循环功能障碍、全身炎症、高凝状态以及中暑期间的脑氧化应激、缺血和损伤。这些发现表明，HRJVF 疗法引起的大脑降温可以通过减轻中暑期间的脑氧化应激、全身炎症、激活的凝血和组织缺血/损伤来使中风患者复苏。
The purpose of the present study was to assess the therapeutic effect of hypothermic retrograde jugular vein flush (HRJVF) on heatstroke. HRJVF was accomplished by infusion of 4 degrees C isotonic sodium chloride solution via the external jugular vein (1.7 mL/100 g of body weight over 5 min). Immediately after the onset of heatstroke, anesthetized rats were divided into 2 major groups and given the following: 36 degrees C or 4 degrees C isotonic sodium chloride solution, i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats was exposed to room temperature (24 degrees C) and used as normothermic controls. When the WC saline-treated rats underwent heat exposure, their survival time values were found to be 23 to 28 min. Immediately after the onset of heatstroke, resuscitation with an i.v. dose of 4 degrees C saline significantly improved survival during heatstroke (208-252 min). All heat-stressed animals displayed systemic inflammation and activated coagulation, evidenced by increased tumor necrosis factor alpha, prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C. Biochemical markers evidenced cellular ischemia and injury/dysfunction: plasma levels of blood urea nitrogen, creatinine, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and alkaline phosphatase; and striatal levels of glycerol, glutamate, and lactate/pyruvate; dihydroxy benzoic acid, lipid peroxidation, oxidized-form glutathione reduced-form glutathione, dopamine, and serotonin were all elevated during heatstroke. Core and brain temperatures and intracranial pressure were also increased during heatstroke. In contrast, the values of mean arterial pressure, cerebral perfusion pressure, and striatal levels of local blood flow, partial pressure of oxygen, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities were all significantly lower during heatstroke. The circulatory dysfunction, systemic inflammation, hypercoagulable state, and cerebral oxidative stress, ischemia, and damage during heatstroke were all significantly suppressed by HRJVF. These findings demonstrate that brain cooling caused by HRJVF therapy may resuscitate persons who had a stroke by attenuating cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke.