Nagasawa S, Kawanishi M, Yamaguchi K, Tada H, Kajimoto S, Kajimoto Y, Tanaka H, Ohta T
Department of Neurosurgery, Osaka Medical College, Takatsuki, Japan.
No Shinkei Geka. 1996 Oct;24(10):897-903.
Obliteration procedures for large high-flow arteriovenous malformations (AVM) were simulated using a compartmental flow model to investigate the role of altered autoregulatory conditions in the development of hyperperfusion and normal perfusion pressure breakthrough (NPPB). Since the arterioles are primarily responsible for autoregulatory function, the role of these structural changes on the development of hyperperfusion was also studied by evaluating the wall thickness (T), internal radius (Ri) and tangential wall stress (sigma). As the AVM flow was decreased during the obliteration procedures, the perfusion pressure (delta P) of the brain tissue surrounding the AVM increased. When the autoregulatory condition was impaired [AR (-)] and the lower limit of the autoregulatory pressure range (LAR) was shifted from 60 mmHg (LAR60) to 40 mm Hg (LAR40), the flow volume in the surrounding brain (Fb) increased markedly, from 67 ml/100g/min to 92 ml/100g/min, with the progress of the obliteration procedures. In these conditions, T/Ri was supposed to be constant and sigma value increased uniformly. In the presence of the autoregulatory mechanism [AR (+)], T/Ri increased against increasing delta P, which resulted in smaller sigma value than that under AR (-) conditions. When the contracted vascular wall yielded on the process of increasing wall stress, delta P and feeder pressure (Pf) decreased to some degree. Concomitantly increase of the sigma value and marked hyperperfusion developed in the brain. The yield of the contracted vascular wall would result in the decrease of a pressure gradient across the arteriole and the reciprocal increase of pressure load on the walls of the capillary and venula, which might lead to NPPB. Since the decrease of delta P or Pf during the progress of the obliterating procedures is considered specific to the appearance of hyperperfusion or NPPB, monitoring these parameters would be useful for its early detection. If the upper limit of the autoregulatory pressure range was assumed to decrease and become the yield point in the brain surrounding high flow AVMs, hyperfusion or NPPB could be considered to develop in the conditions with the autoregulatory pressure range being narrowed and/or shifted to the lower pressure level. Induced systemic hypotension was found to be effective in reducing the magnitude of Fb, delta P, and Pf when induction was appropriately performed in stepwise fashion. T/Ri and sigma were kept in narrow ranges compared to those before induction of hypotension.
使用房室血流模型模拟大型高流量动静脉畸形（AVM）的闭塞过程，以研究自动调节条件改变在高灌注和正常灌注压突破（NPPB）发展中的作用。由于小动脉主要负责自动调节功能，还通过评估壁厚（T）、内径（Ri）和切向壁应力（σ）来研究这些结构变化对高灌注发展的作用。在闭塞过程中，随着AVM血流量减少，AVM周围脑组织的灌注压（ΔP）升高。当自动调节条件受损[AR（-）]且自动调节压力范围的下限（LAR）从60 mmHg（LAR60）变为40 mmHg（LAR40）时，随着闭塞过程的进展，周围脑组织的血流量（Fb）显著增加，从67 ml/100g/min增加到92 ml/100g/min。在这些条件下，假设T/Ri恒定且σ值均匀增加。在存在自动调节机制[AR（+）]的情况下，T/Ri随着ΔP的增加而增加，这导致σ值小于AR（-）条件下的值。当收缩的血管壁在壁应力增加过程中屈服时，ΔP和供血动脉压力（Pf）会有所下降。同时，σ值增加且大脑中出现明显的高灌注。收缩血管壁的屈服会导致小动脉两端压力梯度降低，以及毛细血管和小静脉壁上压力负荷的相应增加，这可能导致NPPB。由于在闭塞过程中ΔP或Pf的降低被认为是高灌注或NPPB出现的特异性表现，监测这些参数将有助于早期检测。如果假设自动调节压力范围的上限降低并成为高流量AVM周围脑组织的屈服点，那么在自动调节压力范围变窄和/或移至较低压力水平的情况下，可能会发生高灌注或NPPB。发现当以逐步方式适当进行诱导时，诱导性全身性低血压可有效降低Fb、ΔP和Pf的幅度。与诱导低血压之前相比，T/Ri和σ保持在较窄范围内。
