Pleşea I E, Cameniţă A, Georgescu C C, Enache S D, Zaharia B, Georgescu Claudia Valentina, Tenovici Mihaela
Department of Pathology, University of Medicine and Pharmacy of Craiova.
Rom J Morphol Embryol. 2005;46(3):249-56.
The study was performed in order to assess the alterations of extra-parenchymal and intraparenchymal vascular structures in 82 hypertensive patients suspected of primary intraparenchymal hematoma, which died and were autopsied in order to confirm the diagnosis.
The studied material consisted of nervous tissue situated near and distant from the haemorrhagic lesion. The specimens of nervous tissue were processed by the classical histological technique and stained with the usual stainings and with immunohistochemical stains for basement membranes and endothelial cells.
Extra-parenchymal arteries showed classic lesions of atherosclerosis. Atheromatous lesions were of all types, even the extension towards the media being encountered a complication with thrombosis. At the level of the intraparenchymal blood vessels, the spectrum of the lesions due to arterial hypertension included all steps of vascular wall degeneration, from hypertrophy of smooth muscle layer to complete hyalinization of arterial wall, but with a focal irregular distribution, not related with the proximity of haemorrhagic focus. High arterial blood pressure also influenced the capillary walls which showed focal or circumferential thickening due to the densification of the type IV collagen material from the basement membrane structure. The CD34 immunostaining showed that endothelial cells kept their structural integrity.
The sequence of degenerative lesions of the cerebral vascular wall culminates with the hyalinization of excessive fibrillar material form arteriolar wall or from basement membranes. Hyalin material is weakening the wall resistance to the stress determined by the high values of blood pressure in hypertension, and, correlated with a minimal resistance of the surrounding cerebral parenchyma, can explain why the cerebral parenchyma is the only tissue in which blood pressure variations can determinate vascular rupture and cerebral haemorrhage. The more adequate term for describing the vascular wall changes seems to be sclerosis (arteriolar and even capillary) with hyalinosis.
本研究旨在评估82例疑似原发性脑实质内血肿的高血压患者的脑实质外和脑实质内血管结构的改变,这些患者死亡后进行尸检以确诊。
研究材料包括位于出血性病变附近和远处的神经组织。神经组织标本采用经典组织学技术处理,并用常规染色以及针对基底膜和内皮细胞的免疫组织化学染色。
脑实质外动脉显示出典型的动脉粥样硬化病变。粥样病变类型多样,甚至可见向中膜扩展并伴有血栓形成的并发症。在脑实质内血管层面,高血压所致病变范围包括血管壁退变的各个阶段,从平滑肌层肥大到动脉壁完全玻璃样变,但分布呈局灶性且不规则,与出血灶的距离无关。高动脉血压还影响毛细血管壁,由于基底膜结构中IV型胶原物质致密化,毛细血管壁出现局灶性或环形增厚。CD34免疫染色显示内皮细胞保持其结构完整性。
脑血管壁退变病变的序列最终导致小动脉壁或基底膜中过多纤维状物质的玻璃样变。玻璃样物质削弱了血管壁对高血压高值所产生应力的抵抗力,并且与周围脑实质的最小抵抗力相关,这可以解释为什么脑实质是唯一血压变化可导致血管破裂和脑出血的组织。描述血管壁变化更恰当的术语似乎是伴有玻璃样变的硬化(小动脉甚至毛细血管)。