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自由基对脑血管通透性和血管舒缩反应的影响。

Effects of free radicals on permeability and vasomotor response of cerebral vessels.

作者信息

Unterberg A, Wahl M, Baethmann A

机构信息

Institut für Chirurgische Forschung, Klinikum Grosshadern, München, Federal Republic of Germany.

出版信息

Acta Neuropathol. 1988;76(3):238-44. doi: 10.1007/BF00687770.

DOI:10.1007/BF00687770
PMID:3213426
Abstract

To obtain further evidence on the role of free radicals as mediators of secondary brain damage, blood-brain barrier (BBB) function and vasomotor response of pial vessels were studied during cortical superfusion of a free radical-generating system of xanthine-oxidase (XO) and hypoxanthine (HX). Intravenously administered Na+-fluorescein (mol. wt. 376), or fluorescein isothiocyanate (FITC)-dextran (mol. wt. 62,000) served as low- and high-molecular weight BBB indicators. Since undialyzed XO considerably increased the osmolarity of artificial cerebrospinal fluid, XO was subjected to equilibrium dialysis, which did not affect enzyme activity. Cortical superfusion with either HX (4 mM) or dialyzed XO alone (0.5 U/ml; osmolarity, 310 mosmol/l) did not induce a vasomotor response. Cortical superfusion with the free radical-generating system under normotonic conditions (HX plus dialyzed XO), led to moderate arterial dilation only with a maximum of +13%. The venous diameters remained unaffected. Moderate extravasation of the low molecular weight indicator Na+-fluorescein was seen in only 33% of the experiments, leakage of FITC-dextran was never observed. To assess the role of hypertonicity of the superfusate, the same experiments were performed with undialyzed XO. When superfusing the cortex with undialyzed XO (0.5 U/ml; osmolarity, 420 mosmol/l), the pial arteries dilated to 146%-168% of normal. Similarly, simultaneous superfusion with undialyzed XO (0.25 U/ml) and HX (2 mM) elicited arterial dilatation to 161%-178% of normal. Even the pial veins were significantly dilated to 108% of normal. In this series a moderate extravasation of Na+-fluorescein occurred in 75%, with leakage of FITC-dextran in 25%.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了获得更多关于自由基作为继发性脑损伤介质作用的证据,在黄嘌呤氧化酶(XO)和次黄嘌呤(HX)自由基生成系统皮质灌注期间,研究了血脑屏障(BBB)功能和软脑膜血管的血管舒缩反应。静脉注射的Na + -荧光素(分子量376)或异硫氰酸荧光素(FITC) - 葡聚糖(分子量62,000)用作低分子量和高分子量BBB指标。由于未透析的XO会显著增加人工脑脊液的渗透压,因此对XO进行了平衡透析,这并不影响酶活性。单独用HX(4 mM)或透析的XO(0.5 U/ml;渗透压,310 mosmol/l)进行皮质灌注未引起血管舒缩反应。在等渗条件下用自由基生成系统(HX加透析的XO)进行皮质灌注,仅导致中等程度的动脉扩张,最大为+13%。静脉直径未受影响。仅在33%的实验中观察到低分子量指示剂Na + -荧光素的中度外渗,从未观察到FITC - 葡聚糖的渗漏。为了评估灌注液高渗的作用,用未透析的XO进行了相同的实验。当用未透析的XO(0.5 U/ml;渗透压,420 mosmol/l)灌注皮质时,软脑膜动脉扩张至正常的146% - 168%。同样,同时用未透析的XO(0.25 U/ml)和HX(2 mM)灌注引起动脉扩张至正常的161% - 178%。甚至软脑膜静脉也显著扩张至正常的108%。在该系列中,75%出现Na + -荧光素的中度外渗,25%出现FITC - 葡聚糖的渗漏。(摘要截断于250字)

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Blood-brain barrier permeability and vascular reactivity to bradykinin after pretreatment with dexamethasone.地塞米松预处理后血脑屏障通透性及血管对缓激肽的反应性
Acta Neuropathol. 1989;77(6):576-81. doi: 10.1007/BF00687884.
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Superoxide dismutase does not prevent delayed hypoperfusion after incomplete cerebral ischaemia in the rat.超氧化物歧化酶不能预防大鼠不完全性脑缺血后的迟发性低灌注。
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Clin Investig. 1992 Mar-Apr;70(3-4):210-7. doi: 10.1007/BF00184653.
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