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长期暴露在热环境下可预防大鼠闭合性颅脑损伤所致的脑损伤。

Long term exposure to heat protects against brain damage induced by closed head injury in the rat.

机构信息

Department of Pharmacology, Hadassah Schools of Pharmacy, Medicine and Dental Medicine, The Hebrew University, Jerusalem, Israel.

出版信息

Restor Neurol Neurosci. 1994 Jan 1;6(2):107-12. doi: 10.3233/RNN-1994-6204.

DOI:10.3233/RNN-1994-6204
PMID:21551737
Abstract

Closed head injury leads to delayed tissue-edema, necrosis and impaired neurological function. In the present study the effect of chronic exposure to heat on the outcome of head injury in rats was investigated. Rats were held at ambient temperature of 24°C (CON) or 34°C (heat acclimated, ACC) for one month, before induction of trauma. Injury was induced by a weight drop device, falling over the left cerebral hemisphere. Twenty-four or 48 h later the rats were sacrificed and their brains removed for evaluation of edema (specific gravity or water content). Blood-brain barrier integrity (Evans blue extravasation) was evaluated 4 h after injury. One, 24 and 48 h after injury the rats were evaluated by a set of criteria which yields their clinical status (Neurological Severity Score - NSS). Forty-eight hours after trauma specific gravity of the contused hemispheres was 1.0389 ± 0.0019 and 1.0364 ± 0.0007 (P < 0.01) and water content 81.44 ± 1.28 and 84.17 ± 1.03% (P < 0.001), for ACC and CON rats, respectively. Lower degree of edema was also evident at 24 h suggesting slower rate of edema formation in ACC rats. Evans blue uptake by the contused hemisphere was 315 ± 61 and 50 ± 23 ng/g tissue in the CON and ACC rats, respectively (P < 0.001). Clinical recovery of the ACC rats was significantly better (P < 0.001) than that of the matched controls as exhibited at 48 h by median NSS values of: 10.8 (range 6-16) and 5 (range 4-6) for CON and ACC, respectively. Based on the present results we suggest that heat acclimation offers protection to rats subjected to head trauma.

摘要

闭合性颅脑损伤导致延迟性组织水肿、坏死和神经功能障碍。本研究探讨了大鼠慢性暴露于热环境对颅脑损伤结局的影响。大鼠在环境温度为 24°C(CON)或 34°C(热适应,ACC)下适应一个月,然后诱导创伤。损伤通过重物下落装置作用于左大脑半球诱发。24 或 48 小时后,处死大鼠并取出大脑评估水肿(比重或含水量)。损伤后 4 小时评估血脑屏障完整性(伊文思蓝渗出)。损伤后 1、24 和 48 小时,通过一套标准评估大鼠的临床状态(神经损伤严重程度评分-NSS)。损伤后 48 小时,挫伤半球的比重分别为 1.0389 ± 0.0019 和 1.0364 ± 0.0007(P < 0.01),含水量分别为 81.44 ± 1.28 和 84.17 ± 1.03%(P < 0.001),ACC 和 CON 大鼠分别。24 小时时水肿程度也较低,表明 ACC 大鼠水肿形成速度较慢。伊文思蓝摄取量分别为 315 ± 61 和 50 ± 23 ng/g 组织(P < 0.001)。ACC 大鼠的临床恢复明显更好(P < 0.001),48 小时时中位数 NSS 值分别为:10.8(范围 6-16)和 5(范围 4-6)。基于目前的结果,我们认为热适应可对颅脑损伤的大鼠提供保护。

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