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实验性高血压大鼠筛状状态的发病机制。

Pathogenesis of état criblé in experimental hypertensive rats.

作者信息

Suzuki K, Masawa N, Takatama M

机构信息

Division of Histopathology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Gunma, Japan.

出版信息

J Stroke Cerebrovasc Dis. 2001 May-Jun;10(3):106-12. doi: 10.1053/jscd.2001.25456.

Abstract

The pathogenesis of état criblé in experimental hypertensive rat brain was studied. Macroscopically, the hypertensive rat brain showed marked subarachnoidal edema. Cystic dilatation of the subarachnoid space, softening, and perivascular dilatation or état criblé, in the caudate putamen, frontoparietal cortex, and basal ganglia were observed by light microscope. Perivascular dilatation was noted not only around the intracerebral arteries and arterioles but also around the veins and venules. Transmission and scanning electron microscopy also confirmed the presence of perivascular dilatation around the same vessels. In addition, transmission electron microscopy confirmed the increased permeability of the endothelial cells in the intracerebral arteries, arterioles, veins, venules, and capillaries of brains with état criblé. Severe medial cell injuries of the arteries and arterioles and edema-induced destruction of the brain around the dilated perivascular space were also observed. Scanning electron microscopy revealed mild or cystic dilatation of the perivascular space, a net-like structure on both sides of the arachnoidal cells resulting in markedly dilated and numerically increased fenestra, and degenerative changes in the perivascular brain tissue. In conclusion, état criblé in experimental hypertensive rat brain results from an increase in perivascular fluid-induced degeneration of the perivascular brain tissue that is in turn induced by an increase in the permeability of blood vessels.

摘要

研究了实验性高血压大鼠脑筛状软化的发病机制。大体上,高血压大鼠脑显示出明显的蛛网膜下腔水肿。光镜下观察到尾状壳核、额顶叶皮质和基底神经节的蛛网膜下腔囊性扩张、软化以及血管周围扩张或筛状软化。血管周围扩张不仅见于脑内动脉和小动脉周围,也见于静脉和小静脉周围。透射电镜和扫描电镜也证实了相同血管周围存在血管周围扩张。此外,透射电镜证实筛状软化脑的脑内动脉、小动脉、静脉、小静脉和毛细血管内皮细胞通透性增加。还观察到动脉和小动脉的严重中层细胞损伤以及扩张的血管周围间隙周围脑的水肿性破坏。扫描电镜显示血管周围间隙轻度或囊性扩张,蛛网膜细胞两侧呈网状结构,导致小孔明显扩张且数量增加,以及血管周围脑组织的退行性改变。总之,实验性高血压大鼠脑的筛状软化是由血管周围液体增加导致血管周围脑组织变性引起的,而血管周围液体增加又是由血管通透性增加所致。

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