Heye N, Paetzold C, Cervós-Navarro J
Institute of Neuropathology, Free University of Berlin, Fed. Rep. of Germany.
Neurosurg Rev. 1991;14(1):7-16. doi: 10.1007/BF00338186.
Ischemic cerebral infarction is caused primarily by occlusion of a large arterial vessel. Local circulatory disturbances in the center of ischemic tissue and in ischemic penumbra and the degree of sensitivity to ischemia in different brain regions influence subsequent ischemic progression. Postischemic recirculation is impaired by hemodynamic disturbances and formation of microthrombi, hemorrheologic changes and degeneratively altered vessels of microcirculation. Increased postischemic coagulation can be demonstrated in laboratory tests of few minutes extending up to two weeks after the onset of ischemia. Morphological observations on microthrombi after experimental focal ischemia as well as in patients with cerebral infarction show that formation of microthrombi is dependent on the duration of ischemia and the extent of infarcted tissue. Microthrombi are most prevalent in early stages of tissue damage. This suggests that microthrombi have an effect on the progression of ischemic necrosis. On the basis of our results, we can state that 1) microcirculatory disturbances are triggered by focal cerebral ischemia, 2) formation of microthrombi is a contributing factor to the evolution of postischemic microcirculatory disturbances, and 3) microthrombi promote the progression of ischemic necrosis.
缺血性脑梗死主要由大的动脉血管闭塞引起。缺血组织中心和缺血半暗带的局部循环障碍以及不同脑区对缺血的敏感程度会影响随后的缺血进展。缺血后再灌注会因血流动力学紊乱、微血栓形成、血液流变学改变以及微循环血管的退行性改变而受损。在缺血发作后几分钟至两周的实验室检查中可证实缺血后凝血增加。对实验性局灶性缺血后以及脑梗死患者的微血栓进行形态学观察表明,微血栓的形成取决于缺血持续时间和梗死组织范围。微血栓在组织损伤早期最为常见。这表明微血栓对缺血性坏死的进展有影响。根据我们的研究结果,我们可以指出:1)局灶性脑缺血引发微循环障碍;2)微血栓形成是缺血后微循环障碍演变的一个促成因素;3)微血栓促进缺血性坏死的进展。