Caner H, Atasever A, Kilinç K, Durgun B, Peker S, Ozcan O E
Department of Neurosurgery, School of Medicine, Hacettepe University, Ankara, Turkey.
Acta Neurochir (Wien). 1993;121(1-2):68-71. doi: 10.1007/BF01405185.
The aetiology of incomplete adrenergic denervation and reduction in the number and caliber of the cerebral vessels in hydrocephalus is still obscure. Stretching of the blood vessels alone is far from explaining these major vascular changes. Previous studies have shown that increased lipid peroxidation produces toxic effects on vessels. This experimental study was designed to investigate the possible aetiology of vascular changes in hydrocephalic rats with special reference to lipid peroxidation. Hydrocephalus was induced by injecting 50 mg/Kg sterilized kaolin suspension into the cisterna magna in 10 rats (Group A). A sham operation was performed for Group B. After three weeks the rats were anaesthetized and perfused transcardially. The brains were dissected, and cut to visualize the degree of hydrocephalus. The arteries of the circle of Willis were removed for light microscopic examination and the brains were kept for the measurement of lipid peroxidation levels. Light microscopic studies of cerebral arteries in hydrocephalic rats revealed spastic vessels with folding and corrugation of the lamina elastica. The level of lipid peroxidation in group A (260 +/- 9.129 nmol TBAR/gr wet tissue) was significantly higher than that of group B (106 +/- 3.59 nmol TBAR/gr wet tissue). It is suggested that vascular changes observed in hydrocephalic rats may be due to the high level of lipid peroxidation, which in turn may be the consequence of ischaemia caused by the hydrocephalus related stretching of cerebral vessels.
脑积水时不完全肾上腺素能去神经支配以及脑血管数量和管径减少的病因仍不清楚。仅血管的拉伸远不能解释这些主要的血管变化。先前的研究表明,脂质过氧化增加会对血管产生毒性作用。本实验研究旨在探讨脑积水大鼠血管变化的可能病因,特别关注脂质过氧化。通过向10只大鼠(A组)的大池内注射50mg/Kg灭菌高岭土混悬液诱导脑积水。对B组进行假手术。三周后,将大鼠麻醉并经心灌注。解剖大脑并切开以观察脑积水程度。取出 Willis 环的动脉进行光镜检查,并保存大脑用于测量脂质过氧化水平。对脑积水大鼠脑动脉的光镜研究显示血管痉挛,弹性膜有折叠和皱纹。A组的脂质过氧化水平(260±9.129nmol TBAR/克湿组织)显著高于B组(106±3.59nmol TBAR/克湿组织)。提示脑积水大鼠观察到的血管变化可能是由于高水平的脂质过氧化,而脂质过氧化反过来可能是脑积水相关脑血管拉伸导致缺血的结果。