1979 年 19 巻 12 号 p. 1149-1156
To make an experimental cerebral infarction in the dog, a proximal clipping of the middle cerebral artery (MCA) was performed and the collateral blood supply was compromised by subjecting the animal hemorrhagic hypotension involving reduction of blood pressure to 50 mmHg for 1 hour. Then, the systemic blood pressure was restored by infusion of the shed blood. The clip was removed at different times—immediately, 0.5 hours, 3 hours, 6 hours, 12 hours and 24 hours after restoration. The no-reflow area was investigated by fluorescein angiography (FAG) and carbon perfusion method (CP). There were other groups in which the clip had been taken off at 0.5 or 4 hours after restoration and circulation was maintained 24 hours. Then the no-reflow area was also investigated.
There was no evidence of the no-reflow phenomenon on the surface vessels after cerebral ischemia in any of the experimental conditions. Arteriovenous shunt or perivascular infiltration of fluorescein dye were only observed in the reflow area in animals which received temporary occlusion of the MCA for 6 hrs or more.
On the other hand, the no-reflow phenomenon was observed by CP in intraparenchymal vessels which had been exposed to focal cerebral ischemia. The longer the duration of ischemia, the more extensive were the areas of non-filling. In animals with recirculation of 24 hrs duration after 4 hrs of temporary occlusion, large perfusion defects were also observed.
In continuous occlusion of the MCA for 24 hrs without removing the clip, extravasation of carbon particles were localized only in the boundary zone between the deep cortical layer and the subcortical white matter. To the contrary, animals with temporary occlusion for 24 hrs or animals with 4 hrs occlusion followed by recirculation for 24 hrs frequently caused wide exudation of carbon particles which extended into the gray matter of the MCA territory. These animals showed more severe hemorrhagic infarction than those with the permanent occlusion.