Baumbach G L, Ghoneim S
University of Iowa College of Medicine, Department of Pathology, Iowa City 52242.
Scanning Microsc. 1993 Mar;7(1):137-42; discussion 143.
Cerebral arterioles in stroke-prone spontaneously hypertensive rats (SHRSP) paradoxically become more distensible, despite hypertrophy of the vessel wall. Cerebral arterioles in SHRSP also undergo remodeling with a reduction in external diameter. Based on these findings, we have proposed the concept that remodeling of cerebral arterioles may be an important mechanism, in addition to hypertrophy, for encroachment on the vascular lumen in SHRSP. The purpose of this review is threefold. First, consequences of vascular hypertrophy that have been proposed previously are reviewed with an emphasis on the hypothesis that encroachment on the vascular lumen by hypertrophy is an important mechanism of altered vascular responses in chronic hypertension. Second, the concept of vascular remodeling is considered with an emphasis on the possibility that remodeling with a reduction in external diameter may contribute importantly to altered cerebral vascular responses in SHRSP. Finally, possible mechanisms of vascular remodeling are considered with an emphasis on the hypothesis that a reduction in external diameter may be related to a decrease in the length of individual smooth muscle cells without an increase in cell number, or an increase in the number of times each smooth muscle cell wraps around the arteriole.
在易患中风的自发性高血压大鼠(SHRSP)中,尽管血管壁肥厚,但脑小动脉却反常地变得更具扩张性。SHRSP的脑小动脉还会发生重塑,外径减小。基于这些发现,我们提出了这样一个概念:除了肥厚之外,脑小动脉的重塑可能是SHRSP中血管腔被侵占的一个重要机制。本综述有三个目的。首先,回顾先前提出的血管肥厚的后果,重点关注肥厚导致血管腔被侵占是慢性高血压中血管反应改变的重要机制这一假说。其次,考虑血管重塑的概念,重点关注外径减小的重塑可能对SHRSP中脑血管反应改变有重要贡献的可能性。最后,考虑血管重塑的可能机制,重点关注外径减小可能与单个平滑肌细胞长度减少而细胞数量不增加,或每个平滑肌细胞围绕小动脉缠绕次数增加有关的假说。