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建立并评估高原脑水肿实验动物模型。

Establishment and evaluation of an experimental animal model of high altitude cerebral edema.

机构信息

Department of High Altitude Diseases, College of High Altitude Military Medicine, Third Military Medical University, Chongqing 400038, China.

出版信息

Neurosci Lett. 2013 Jun 28;547:82-6. doi: 10.1016/j.neulet.2013.05.008. Epub 2013 May 14.

DOI:10.1016/j.neulet.2013.05.008
PMID:23680461
Abstract

The aim of our study was to develop a model of high altitude cerebral edema (HACE) using an acute, hypobaric hypoxia environment combined with exhaustive exercise. Forty healthy male Sprague-Dawley rats were randomly divided into a plains control group (PC group) and a plateau altitude hypoxia group (AH group). After 2 days of treadmill adaptation under normoxic conditions, the AH group was housed in hypobaric conditions (simulating 4000 m above sea level) for 2 days while performing exhaustive exercise. The simulated altitude was then increased to 8000 m for 3 days of simple hypobaric hypoxia exposure. Compared with the PC group, the AH group showed significantly greater (P<0.01) water content and Evans blue staining in their brain tissue. Furthermore, the hippocampal formation was seriously damaged, and the number of pyramidal cells decreased. In addition, the brain structure was altered into a loose state with notable edema, which was demonstrated by the leakage of lanthanum nitrate particles from brain microvessels into the surrounding tissue through widened tight junctions. Some neurons and glial cell organelles were swollen and some nerve fibers were demyelinated as well. We have shown that acute hypobaric hypoxia exposure with exhaustive exercise increases the permeability of the blood-brain barrier and leads to cerebral edema, making this a valid animal model of HACE.

摘要

本研究旨在建立一种高原脑水肿(HACE)模型,采用急性低压缺氧环境与力竭运动相结合的方法。将 40 只健康雄性 Sprague-Dawley 大鼠随机分为平原对照组(PC 组)和高原缺氧组(AH 组)。在常氧条件下进行 2 天跑步机适应后,AH 组在低压环境下(模拟海拔 4000 米)居住 2 天,同时进行力竭运动。然后将模拟海拔升高至 8000 米,进行 3 天单纯低压缺氧暴露。与 PC 组相比,AH 组脑组织的含水量和伊文思蓝染色明显增加(P<0.01)。此外,海马结构严重受损,锥体细胞数量减少。此外,脑结构改变为疏松状态,明显水肿,通过增宽的紧密连接,硝酸镧颗粒从脑微血管漏入周围组织。一些神经元和神经胶质细胞细胞器肿胀,一些神经纤维脱髓鞘。我们已经表明,急性低压缺氧暴露与力竭运动增加了血脑屏障的通透性,导致脑水肿,这是 HACE 的一种有效的动物模型。

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