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大鼠缺氧后脑水肿中血脑屏障对蛋白质的通透性

The permeability of the blood-brain barrier to protein in the post-hypoxic cerebral edema of the rat.

作者信息

Ushijima K, Ogata K, Miyazaki H, Morioka T

出版信息

Resuscitation. 1984 Nov;12(3):167-74. doi: 10.1016/0300-9572(84)90002-9.

Abstract

The permeability of the blood-brain barrier to protein was studied in the post-hypoxic cerebral edema of rats, using horseradish peroxidase (HRP) as a tracer protein. Under halothane anesthesia, HRP was injected intravenously. Then the animals were exposed to hypoxic-ischemia by inhalation of 5% oxygen in nitrogen and temporary occlusion of the left common carotid artery for 10-30 min. Twenty-four, 48 or 72 h after the hypoxic experiments, the animals were anesthetized with sodium pentobarbital and their body tissues were fixed by perfusion with a mixture of glutaraldehyde and p-formaldehyde before the autopsy. No brain edema was observed in the animals exposed to hypoxia for 10 min, but the animals exposed to hypoxia for 20-30 min revealed a left hemispheric brain edema. The brain was immediately immersed in the same fixatives, and then sectioned with a cryostat. The sections were stained histochemically according to the method of Graham and Karnovsky (1966) to identify the distribution of the HRP. HRP was not found even in the edematous hemisphere. In this type of brain edema, it is suggested that there was no acceleration of permeability of blood-brain barrier to serum proteins whose molecular weights were larger than HRP, and therefore it would have no causative relationship with the production of brain edema.

摘要

以辣根过氧化物酶(HRP)作为示踪蛋白,研究了大鼠缺氧后脑水肿时血脑屏障对蛋白质的通透性。在氟烷麻醉下,静脉注射HRP。然后通过吸入含5%氧气的氮气并暂时阻断左颈总动脉10 - 30分钟使动物暴露于缺氧缺血状态。缺氧实验后24、48或72小时,用戊巴比妥钠麻醉动物,在尸检前通过灌注戊二醛和多聚甲醛的混合物固定其身体组织。暴露于缺氧10分钟的动物未观察到脑水肿,但暴露于缺氧20 - 30分钟的动物出现左半球脑水肿。将大脑立即浸入相同的固定剂中,然后用低温恒温器切片。根据Graham和Karnovsky(1966年)的方法对切片进行组织化学染色以确定HRP的分布。即使在水肿半球也未发现HRP。在这种类型的脑水肿中,提示血脑屏障对分子量大于HRP的血清蛋白的通透性没有加快,因此它与脑水肿的产生没有因果关系。

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