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高容量血液稀释对中暑大鼠脑内谷氨酸、甘油、乳酸及自由基的影响。

Effect of hypervolaemic haemodilution on cerebral glutamate, glycerol, lactate and free radicals in heatstroke rats.

作者信息

Chang Chen-Kuei, Chiu Wen-Ta, Chang Ching-Ping, Lin Mao-Tsun

机构信息

Division of Neurosurgery, Department of Surgery, Mackay Memorial Hospital, Taipei, Taiwan.

出版信息

Clin Sci (Lond). 2004 May;106(5):501-9. doi: 10.1042/CS20030263.

Abstract

In the present study, we attempted to assess the mechanisms underlying the neuroprotective effect of hypervolaemic haemodilution in rat heatstroke. In anaesthetized rats treated with normal saline (NS) immediately after the onset of heatstroke induced by T (a) (ambient temperature) of 42 degrees C for 88 min, followed by T (a) of 24 degrees C for 12 min, the values for MAP (mean arterial pressure), ICP (intracranial pressure), CPP (cerebral perfusion pressure), CBF (cerebral blood blow), brain P O(2) (partial pressure of O(2)) and striatal glutamate, glycerol, lactate/pyruvate ratio, hydroxyl radicals and neuronal damage score were 42+/-3 mmHg, 33+/-3 mmHg, 9+/-3 mmHg, 109+/-20 BPU (blood perfusion units), 6+/-1 mmHg, 51+/-7 micromol/l, 24+/-3 micromol/l, 124+/-32, 694+/-22% of baseline and 2.25+/-0.05 respectively. In animals treated with 10% albumin immediately after the onset of heatstroke ( T (a) of 42 degrees C for 88 min), the values for MAP, ICP, CPP, CBF, brain P O(2) and striatal glutamate, glycerol, lactate/pyruvate ratio, hydroxyl radicals and neuronal damage score were 64+/-6 mmHg, 10+/-2 mmHg, 54+/-5 mmHg, 452+/-75 BPU, 15+/-2 mmHg, 3+/-2 micromol/l, 4+/-2 micromol/l, 7+/-3, 119+/-7% of baseline and 0.38+/-0.05 respectively. Apparently, the heatstroke-induced arterial hypotension, intracranial hypertension, cerebral hypoperfusion, cerebral ischaemia, brain hypoxia, increased levels of striatal glutamate, glycerol, lactate/pyruvate ratio and hydroxyl radicals, and increased striatal neuronal damage score values were all attenuated significantly by the induction of hypervolaemic haemodilution in rats immediately at the onset of heatstroke. These results demonstrate that the neuroprotective effect of hypervolaemic haemodilution is associated with a decrease in the elevation of glutamate, glycerol, lactate and free radicals in brain exposed to experimental heatstroke-induced cerebral ischaemia/hypoxia injury.

摘要

在本研究中,我们试图评估大鼠中暑时高容量血液稀释神经保护作用的潜在机制。在通过将环境温度(Ta)设为42℃持续88分钟诱导中暑发作后立即用生理盐水(NS)处理的麻醉大鼠中,随后将Ta设为24℃持续12分钟,平均动脉压(MAP)、颅内压(ICP)、脑灌注压(CPP)、脑血流量(CBF)、脑氧分压(PO₂)以及纹状体谷氨酸、甘油、乳酸/丙酮酸比值、羟自由基和神经元损伤评分的值分别为42±3 mmHg、33±3 mmHg、9±3 mmHg、109±20血流灌注单位(BPU)、6±1 mmHg、51±7 μmol/L、24±3 μmol/L、124±32、为基线的694±22%以及2.25±0.05。在中暑发作(Ta为42℃持续88分钟)后立即用10%白蛋白处理的动物中,MAP、ICP、CPP、CBF、脑PO₂以及纹状体谷氨酸、甘油、乳酸/丙酮酸比值、羟自由基和神经元损伤评分的值分别为64±6 mmHg、10±2 mmHg、54±5 mmHg、452±75 BPU、15±2 mmHg、3±2 μmol/L、4±2 μmol/L、7±3、为基线的119±7%以及0.38±0.05。显然,中暑诱导的动脉低血压、颅内高压、脑灌注不足、脑缺血、脑缺氧、纹状体谷氨酸、甘油、乳酸/丙酮酸比值和羟自由基水平升高以及纹状体神经元损伤评分值增加,在中暑发作时立即对大鼠进行高容量血液稀释诱导后均显著减轻。这些结果表明,高容量血液稀释的神经保护作用与暴露于实验性中暑诱导的脑缺血/缺氧损伤的大脑中谷氨酸、甘油、乳酸和自由基升高的降低有关。

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