抄録
Experimental cerebral infarction was induced in 94 dogs by injecting one or two silicone rubber cylinders through the cervical internal carotid artery. The 47 large-sized infarctions of the cerebral hemisphere (LSICH) were more frequently created with a double silicone embolization (DSE; 76.2%) than with a single silicone embolization (42.5%). In the DSE method, the first embolization gave rise to an occlusion of the proximal segment of the middle cerebral artery. The lenticulostriate arteries were also occluded directly. With the second embolization, a point occlusion of the orifice of the posterior communicating and/or anterior cerebral arteries occurred, but the perforators from these arteries were not occluded directly. Therefore, the LSICH model showed widespread infarction, involving the basal ganglia, the cortex, and the white matter in the territory of the middle cerebral artery. The massive hemorrhagic area in this LSICH model tended to be localized in the basal ganglia (10.4%). Similarly, red softening was localized in the corticomedullary junctional area (89.6%) and pale softening, in the boundary zone between the middle and posterior cerebral arteries (39.6%), respectively.
From histopathological examination, it was also suggested that the massive hemorrhagic area might be caused by disruption of arterioles in the perforating arterial terminal zone. By contrast, the red softening area was due to disruption of the venules in the cortical arterial terminal zone.
Pathogenetic mechanisms of the location of three types of infarction in LSICH model are also discussed.
