Experimental Cerebral Infarction in the Dog : 1.Pathogenesis of Hemorrhagic Infarction

1. The middle cerebral artery of dogs was occluded by a clip and the collateral blood supply was compromised by subjecting to hemorrhagic hypotension for I hour. Following restoration of the systemic blood pressure by infusion of the shed blood, changes in an area of ischemia was investigated chiefly by fluorescein angiography (FAG) through the lingual artery and the femoral vein and by carbon perfusion (CP) through the heart. The involved cerebral tissue showed to marked hemorrhagic infarction 24 hours after restoration of the blood pressure.2. Figure 1 demonstrated the capillary network in the normal canine brain by FAG and CP. During period of the early three hours after restoration of blood pressure to normal, patchy non-filling area by carbon black was observed within the cortex which surface showed complete or incomplete ischemia by FAG (Fig.2). By six hours,a statistically significant increase in the ischemic area of the cerebral cortex was demonstrated in the territory of the clipped artery and edema could then be demonstrated in the affected cerebral tissue (Fig.3). After twelve hours, diapedesis and extravasation of carbon particles had resulted from permeability changes in dilated long perforating vessels (Fig.4) and within 24 hours the involved cerebral tissue showed marked hemorrhagic infarction which massive amount of extravasated carbon particles localized in the boundary zone between the deep cortical layer and the subcortical white matter (Fig.6)