摘要
建立了一个新的非定常脑AVM血液动力学模型.模型克服了以往的定常AVM模型无法反映血流实际脉动,以及模型结构和血管性质描述上的缺陷,并依据临床实测数据提出了一种更为符合生理和病理实际的描述AVM供血动脉扩张现象的方法.模型模拟了AVM造成的脑血管压力、流量波形和脑血管输入阻抗的变化,并对脑AVM病人脑血管系统的输入阻抗进行了分析.为研究具有复杂结构的脑AVM血液动力学的特征,提供了一个有效的工具.
A novel unsteady hemodynamic model of the cerebral arteriovenous malformation(AVM) is proposed. The major improvements of the novel model include the introduction of the pulsatile nature of blood flow into the systemic hemodynamic investigation of cerebral AVM for the first time and the proposal of a reasonable mechanism for feeding artery dilation based on the authors' first-hand measurements, which has not been appropriately described in the previous models. The model can be used to study cerebral AVM hemody-namincs of various vascular structures from either global or local viewpoint. Thus it should serve as a useful theoretical tool for hemodynamic investigation of the cerebral AVMs pathology, embolization therapy, and it should also serve for individual cases that are difficult of diagnoising and treating due to complicated vascular structure.
With this model, the changes of pressure and flow rate wave and the input impedance of the cerebral vascular system caused by the cerebral AVM are simulated. Through the analysis of simulation and clinic measured data, the following findings are obtained: 1) Feeding artery dilation is an important factor for a cerebral AVM hemodynamic model. Inappropriate description of this pathological phenomina phenomena will lead to variance of input impedance between the model and the true cerebral vascular system. 2) The change between the average value and the peak value of pressure wave in AVM feeding arteries is not consistent. The change of systolic peak value is notablely greater than that of the average value after simulate embolization. 3) The decrease of both the peripheral resistance and characteristic impedance is an important characteristic of the cerebral vascular system in cerebral AVM patients. The decrease of the peripheral resistance is attributed to the low resistance of AVM vessels while that of the characteristic impedance is attributed to the increase of the feeding artery diameter. This result provides a theoritical basis for exploring the pathologic
出处
《力学学报》
EI
CSCD
北大核心
2003年第5期524-532,共9页
Chinese Journal of Theoretical and Applied Mechanics
基金
国家自然科学基金(39870228)
