Mathematical simulation of cerebral blood flow in focal ischemia.
Mathematical simulation of cerebral blood flow in focal ischemia.
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局灶性缺血时脑血流的数学模拟。
DOI：
10.1161/01.str.13.5.693
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发表时间：
1982
期刊：
影响因子：
8.3
通讯作者：
Reneau,DD
中科院分区：
文献类型：
--
作者：
Hudetz,AG;HalseyJr,JH;Horton,CR;Conger,KA;Reneau,DD
建立了一个计算机模型来描述大脑中动脉闭塞引起的局灶性缺血过程中局部脑血流和组织氧合的自动调节。该稳态模型描述了脑动脉系统的血流分布，包括威利斯环和枕动脉吻合口，并包括一种简化形式的自动调节，分别基于枕动脉和脑内动脉的局部压力和流量控制。用该模型进行的初步模拟研究得出了以下结果。在局灶性缺血低血压状态下，模型预测自动调节效果较差。动脉血管的被动扩张使自调节曲线向左移动。MCA闭塞的模拟结果显示，在包括特别脆弱的纹状体区域在内的缺血区域，吻合头在提供充足的血液和氧气供应方面具有重要意义。当吻合口直径为80微米时，并发Krogh圆柱体模型估计mca皮质缺血脑组织（pO2小于1 mmHg）体积为50%，缺血区在直径为170微米时消失。吻合口相对较小（小于200米），该模型在脑血管舒张过程中表现出脑内偷窃。包括吻合动脉在内的枢轴动脉被动扩张导致血流消失和逆转。这些结果表明，自体调节转移和偷反转都可以通过被动扩张的血管来解释。
A computer model was developed to describe regional cerebral blood flow and tissue oxygenation with autoregulation during focal ischemia produced by occlusion of th middle cerebral artery (MCA). This steady state model described the distribution of blood flow in the cerebral arterial system including the circle of Willis as well as the pial arterial anastomoses, and included a simplified form of autoregulation based on the local control of pressure and flow in the pial and intracerebral arteries, respectively. Preliminary simulation studies with the model yielded the following results. Less effective autoregulation was predicted by the model at low blood pressure in focal ischemia. Passive dilatation of the pial vasculature produced a leftward shift in the autoregulatory curve. Simulations with occlusion of the MCA revealed the ultimate importance of the pial anastomoses in providing adequate blood and oxygen supply in the ischemic territories including the specially vulnerable lenticulostriate area. The volume of the ischemic (pO2 less than 1 mmHg) brain tissue in the MCA-cortex estimated by using a concurrent Krogh cylinder model was 50% when the pial anastomoses were 80 micrometers in diameter and the ischemic area disappeared at 170 micrometers diameter. With relatively small anastomoses (less than 200 m) the model demonstrated intracerebral steal during intracerebral vasodilation. Passive dilation of the pial arteries including the pial anastomoses caused the steal to disappear and to reverse. These results suggest that both autoregulatory shift and steal reversal can be explained by passive dilatation of the pial vasculature.
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