Abstract
Twenty healthy mongrel dogs weighing 8 to 15 kg were used in this study. As an experimental model of cerebral infarction, the right common, internal, and external carotid arteries were dissected and silastic cylindrical emboli (diameter: 1.1 mm, length: 6-7 mm) were introduced through the right internal carotid artery to the right middle cerebral artery under pentobarbital anesthesia (25 mg/kg of body weight). The emboli reached the proximal portion of the right middle cerebral artery and occlusion of this site was obtained in each dog except for one case. Following this method, right hemispheric cerebral ischemic lesions were observed in 19 dogs.
CT scans (EMI 1010) were performed at an interval of a week after the occlusion of the artery. Low density areas were noticed in CT scans of 19 dogs. In 16 out of 19 cases, positive contrast enhancement (CE) was noted.
Five out of the 16 dogs had positive CE in the acute stage after the arterial occlusion and all of these five dogs showed typical hemorrhagic infarction histologically. There were marked hemorrhages and perivascular edema in the infarcted area microscopically. These findings suggested that the positive CE in the acute stage may be attributed to extravasation of contrast medium following opening or damage of the blood brain barrier (BBB) in the infarcted area.
Positive CE in the chronic stage was seen in the remaining 11 dogs. The positive CE appeared seven or more days after the surgery on the arterial occlusion. In these cases numerous new capillaries, macrophages and reticulin fibers were seen in the infarcted area microscopically. Evans blue solution was administered intravenously before sacrifice and marked extravasation of the dye was seen in the region where the positive CE was noted. Electron microscopically, numerous pinocytotic vesicles and microvacuoles were seen in the hypertrophic cytoplasm of the endothelium. However, no opening of the tight junction between the endothelial cells was seen. These findings suggested that the positive CE in the chronic stage was caused by extravasation of contrast medium by active pinocytotic vesicles through the newly formed vessels for scavenging infarcted cerebral tissue.
