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Effects of cerebral hypothermia on brain tissue impedance and extracellular ion concentrations

脑低温对脑组织阻抗和细胞外离子浓度的影响

基本信息

批准号：
10671320
负责人：
MORI Kentaro
金额：
$ 0.83万
依托单位：
Juntendo University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671320/
关键词：
hypothermia cerebral ischemia glutamate vasoconstriction brain impedance extracellular ion water channel ion channel

项目摘要

The purpose of this research project was to investigate the protective mechanismas of cerebral hypothermia and to improve its therapeutic effects.1. Effects of cerebral hypothermia on cerebral blood flow and metabolismWe investigated the effects of hypothermia on cerebral blood flow (CBF) and metabolism (CMROィイD22ィエD2, AVDOィイD22ィエD2), cerebral venous oxygen saturation (ScvOィイD22ィエD2), cerebral blood volume (CBV), and cerebral vascular resistance (CVR) using 34 anesthetized cat. Brain temperature was controlled from 37 to 25℃. AVDOィイD22ィエD2 increased significantly at 29℃, ScvOィイD22ィエD2 decreased significantly at 29℃, CBV decreased significantly at 29℃, and CVR increased significantly at 29℃. The combined effect of hypothermia with vasopressor (noradrenalin) administration improved all these metabolic parameters. These results suggest that hypothermia below 30℃ may cause cerebral vasoconstriction and misery perfusion in the brain. This potential risk of relative ischemia can be avoided b … More y combination with vasopressor administration.2. Effects of cerebral hypothermia on brain tissue impedane and extracellular ion concentrationsWe investigated the effects of mild cerebral hypothermia on brain tissue impedance (brain extracellular space: ECS) and extracellular ion concentrations ([NaィイD1+ィエD1] ィイD2eィエD2, [KィイD1+ィエD1] ィイD2eィエD2) under cerebral ischemia using anesthetized 11 rats. After global ischemia, ECS began to decrease (post-ischemic cell swelling) at 32±5 sec and then [NaィイD1+ィエD1] ィイD2eィエD2 started to decrease (NaィイD1+ィエD1 ion influx into cells) at 83±30 sec. Hypothermia significantly prolonged both changes of ECS and extracellular ion concentrations. These result shows that cerebral ischemic cell swelling start to occur earlier than extracellular NaィイD1+ィエD1 ion influx into cells. This fact makes it difficult to explain the mechanism of the cell swelling by the former theory that swelling is caused by isotonic water movement after NaィイD1+ィエD1 influx. It is suggested that a depletion of intracellular ATP causes dephospholization of water channel (aquaporin 4) and directly open this water channel. Cerebral hypothermia may influence this water channel directly and prolong the opening of this water channel. Less

本研究旨在探讨脑低温的保护机制，提高脑低温的治疗效果.脑低温对脑血流量和代谢的影响我们用34只麻醉猫观察了脑低温对脑血流量（CBF）、脑代谢（CMRO脑血流D22）、脑静脉血氧饱和度（ScvO脑血流D22）、脑血容量（CBV）和脑血管阻力（CVR）的影响。29℃时AVDO呼吸道D22呼吸道D2显著升高，29℃时ScvO呼吸道D22呼吸道D2显著降低，29 ℃时CBV显著降低，29℃时CVR显著升高。低温与血管加压素（去甲肾上腺素）管理的综合作用改善了所有这些代谢参数。提示30℃以下低温可引起脑血管收缩和脑灌注不良。这种相对缺血的潜在风险可以避免B ...更多信息 y与血管加压药联合给药。脑低温对脑组织阻抗和细胞外离子浓度的影响采用11只麻醉大鼠，观察了亚低温对脑缺血时脑组织阻抗（脑细胞外间隙：ECS）和细胞外离子浓度（[Na ~+ D_1 + Na ~+ D_1] Na ~+ D_2e ~+ D_2，[K ~+ D_1 + Na ~+ D_1] Na ~+ D_2e ~+ D_2）的影响。全脑缺血后，ECS在32±5秒开始减少（缺血后细胞肿胀），然后[Na + D1+ Na + D1]+ D2 + D2在83±30秒开始减少（Na + D1+ Na + D1离子流入细胞）。低温显著延长了ECS和细胞外离子浓度的变化。这些结果表明，脑缺血细胞肿胀开始发生早于细胞外Na + D1+ D1离子流入细胞。这一事实使得难以用先前的理论解释细胞溶胀的机制，即溶胀是由Na + D1+ D1内流后的等渗水运动引起的。这表明细胞内ATP的耗竭导致水通道（水通道蛋白4）的去磷酸化并直接打开该水通道。脑低温可直接影响该水通道，延长该水通道的开放时间。少