Johansson B B, Fredriksson K
J Cardiovasc Pharmacol. 1985;7 Suppl 2:S90-3.
Chronic hypertension is associated with structural alterations in the cerebrovascular bed, with increased vessel wall thickness and media/lumen ratio over a large range of arterial sizes. In the relaxed cortical surface arteries of spontaneously hypertensive rats and in some segments of the basal arteries, the enlarged media encroaches on the lumen. The altered vessel geometry increases the steepness of the resistance curve and enables the blood vessels to withstand higher intraluminal pressure. On the other hand, the risk for ischemic complications is increased because of an elevated minimal resistance. Pathological, degenerative changes occur when the compensatory mechanisms are insufficient to protect the microvessels from the pressure increases. Small intraparenchymatous cerebral arteries develop hyaline degeneration, fibrinoid necrosis, and microaneurysms with the appearance of hemorrhages and lacunae. Hypertension predisposes for atherosclerosis in the cervicocranial and intracranial basal arteries, increasing the risk for large hemispheric infarcts and transitory ischemic attacks. Stenosis/occlusion of the arteries and embolization from an atheromatous plaque might have a larger impact on the hypertensive than the normotensive brain because of less efficient collateral circulation related to the altered vessel geometry.
慢性高血压与脑血管床的结构改变有关,在大范围的动脉管径中,血管壁厚度增加,中膜/管腔比值增大。在自发性高血压大鼠的舒张期皮质表面动脉以及基底动脉的某些节段,增厚的中膜会侵占管腔。血管几何形状的改变增加了阻力曲线的斜率,使血管能够承受更高的管腔内压力。另一方面,由于最小阻力升高,缺血性并发症的风险增加。当代偿机制不足以保护微血管免受压力升高的影响时,就会发生病理性、退行性改变。脑实质内的小动脉会出现透明变性、纤维蛋白样坏死和微动脉瘤,并伴有出血和腔隙形成。高血压易导致颈颅和颅内基底动脉发生动脉粥样硬化,增加大脑半球大面积梗死和短暂性脑缺血发作的风险。由于血管几何形状改变导致侧支循环效率降低,动脉狭窄/闭塞和动脉粥样硬化斑块的栓塞对高血压患者大脑的影响可能比对血压正常者的大脑更大。