Experimental cerebral infarction in the dog (Part 5). Four categories of infarction (author's transl)

Abstract

Experimental cerebral infarction was induced in dogs by injecting one or two silicone rubber cylinders through the cervical internal carotid artery. Twenty-four hours after embolization, the animals were sacrificed and changes of microvessels in the hemispheric infarct were investigated by the electron microscope. In addition to the usual ultrathin sectioning method, the vascular casting method using Mercox® in combination with the cryofracture method, and the freeze-fracture replica method were also used. Gross specimens and histologic sections revealed that massive hemorrhagic areas were localized in the region of basal ganglia and petechial hemorrhages were observed in the corticomedullary junctional region of the affected hemisphere in the middle cerebral artery distribution. In ultrathin sections of arterioles obtained from the infarcted area of the basal ganglia, vacuolations and bleb-formations of the degenerative endothelial cells and smooth muscle cells, and duplications and fragmentations of the basal lamina appeared, while numerous red blood cells and fibrin materials were observed in the dilated subarachnoid space. In vascular casts of these 50, um diameter arterioles, aneurysm-like dilatations were observed at their bifurcations, where numerous red blood cells and Mercox® massively extravasated through the disrupted wall in the necrotized neuropils. Red blood cells in the dilated subarachnoid space were observed in the ultrathin sections of venules in the corticomedullary junctional region, but the degenerative changes were mild. In vascular casts of venules, leakage of Mercox® was observed around the adventitia. It is suggested that a massive hemorrhagic infarction was caused by the disruption of arterioles in the perforating arterial terminal zone and petechial hemorrhagic infarction was caused by the disruption of venules in the cortical arterial terminal zone. No opening of tight junctions was recognized in the ultrathin sections of capillary endothelial cells in the ischemic cerebral cortex, but pinocytotic vesicles increased. In freeze-fracture replicas of capillary endothelia of both normal and ischemic cerebral cortices, tight junctions were seen as a network of ridges, composed of about 100 A particles on the protoplasmic (p) face and grooves on the exoplasmic (e) face. Pinocytotic vesicles were seen as invaginations on the p face and as protrusions on the e face. The average number of pinocytotic vesicles per μm2 was 7 on the luminal front in the normal cortex and 28 in the ischemic cortex. The size of pinocytotic vesicles was 0.62 X10-2 μm on the p face of the normal cortex and 0.83×10-2μm on the p face of the ischemic cortex. It is suggested that pinocytotic vesicles had a more important role in the increase of permeability in the cerebral capillary endothelial cells of the ischemic brain.