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高血压大鼠脑血管对辣根过氧化物酶的通透性:单侧蓝斑损毁的影响

Cerebrovascular permeability to horseradish peroxidase in hypertensive rats: effects of unilateral locus ceruleus lesion.

作者信息

Nag S, Harik S I

出版信息

Acta Neuropathol. 1987;73(3):247-53. doi: 10.1007/BF00686618.

Abstract

Unilateral locus ceruleus lesion enhances leakage of radioiodinated human serum albumin into the ipsilateral cerebral cortex of rats with norepinephrine-induced hypertension. This ultrastructural study was undertaken, to determine the mechanism by which this permeability alteration occurs, using horseradish peroxidase (HRP) as a tracer. Unilateral locus ceruleus lesion was produced in male Wistar-Furth rats by stereotaxic microinfusion of 5 micrograms of 6-hydroxydopamine. Two weeks later, rats were injected with HRP intravenously and acute hypertension was induced in awake rats by an intravenous infusion of norepinephrine (6 micrograms), epinephrine (6 micrograms) or angiotensin amide (12 micrograms) given over a 2-min period. Thirty seconds later, the rats were perfused with fixative under deep anesthesia and their brains were sliced and processed for demonstration of HRP reaction product. Leakage of HRP occurred in both cerebral hemispheres in response to hypertension induced by the three pressor agents, but the leakage was greater on the lesioned side in response to epinephrine and norepinephrine, while in the case of angiotensin-induced hypertension side-to-side differences in permeability alterations were not observed. In both cerebral hemispheres increased permeability affected mainly arterioles, which showed enhanced pinocytosis as the principal mechanism of HRP extravasation.

摘要

单侧蓝斑损伤会增强放射性碘化人血清白蛋白向去甲肾上腺素诱导高血压大鼠同侧大脑皮质的渗漏。本超微结构研究旨在利用辣根过氧化物酶(HRP)作为示踪剂,确定这种通透性改变发生的机制。通过立体定向微量注射5微克6-羟基多巴胺,在雄性Wistar-Furth大鼠中制造单侧蓝斑损伤。两周后,给大鼠静脉注射HRP,并在2分钟内通过静脉输注去甲肾上腺素(6微克)、肾上腺素(6微克)或血管紧张素酰胺(12微克)在清醒大鼠中诱导急性高血压。30秒后,在深度麻醉下用固定剂灌注大鼠,将其大脑切片并进行处理以显示HRP反应产物。三种升压剂诱导高血压时,HRP在双侧大脑半球均有渗漏,但对肾上腺素和去甲肾上腺素反应时,损伤侧的渗漏更大,而在血管紧张素诱导的高血压情况下,未观察到通透性改变的双侧差异。在双侧大脑半球,通透性增加主要影响小动脉,小动脉显示出增强的胞饮作用是HRP外渗的主要机制。

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