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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

本课题的研究目的是探讨脑低温的保护机制并提高其治疗效果。 1．脑低温对脑血流量和代谢的影响我们研究了低温对脑血流量（CBF）和代谢（CMROiiD22ィエD2、AVDOiiD22ィエD2）、脑静脉氧饱和度（ScvOiiD22ィエD2）、脑血容量（CBV）和使用 34 只麻醉猫进行脑血管阻力 (CVR)。脑温度控制在37～25℃。 AVDOィイD22ィエD2在29℃时显着上升，ScvOィイD22ィエD2在29℃时显着下降，CBV在29℃时显着下降，CVR在29℃时显着上升。低温与血管升压药（去甲肾上腺素）联合作用改善了所有这些代谢参数。这些结果表明，30℃以下的低温可能会导致脑血管收缩和大脑灌注不良。与血管加压药联合使用可以避免这种相对缺血的潜在风险。2。脑低温对脑组织阻抗和细胞外离子浓度的影响我们研究了轻度脑低温对脑组织阻抗（脑细胞外间隙：ECS）和细胞外离子浓度（[NaィイD1+ィエD1]ィイD2eエD2，[KィイD1+ィD1]的影响ィイD2eィエD2)脑下使用麻醉的 11 只大鼠进行缺血。整体缺血后，ECS在32±5秒时开始减少（缺血后细胞肿胀），然后[NaィイD1+ィエD1]ィイD2eィエD2在83±30秒开始减少（NaィイD1+ィエD1离子流入细胞）。低温显着延长了 ECS 和细胞外离子浓度的变化。这些结果表明，脑缺血细胞肿胀早于细胞外NaiiD1+iiD1离子流入细胞内开始发生。这一事实使得之前的理论认为细胞肿胀是NaaiD1+ィD1流入后等渗水运动引起的，从而难以解释细胞肿胀的机制。据推测，细胞内 ATP 的消耗会导致水通道（水通道蛋白 4）去磷酸化并直接打开该水通道。脑低温可能会直接影响该水道并延长该水道的开放时间。较少的