抄録
Experimental cerebral infarction was produced in dogs by injecting one or two silicone rubber cylinders through the cervical internal carotid artery (permanent group). In some dogs the rubber cylinder was removed by pulling out the monofilament suture thread after 6 hours of temporary embolization (temporary group). Twenty-four hours after embolization, the animals were killed.
In ultrathin section of capillary endothelium in the ischemic cerebral cortex of both groups, surface infolding and increase in number of pinocytotic vesicles were recognized, but no findings of opening of tight junctions were ascertained.
In replica preparations of both groups, no definite findings of opening junctions were certificated. Pinocytotic vesicles were seen as invaginations on the protoplasmic face and as protrusions on the extracellular face. The average number per square μm was increased. On the luminal front of protoplasmic face, it reached to 28±6 equally in both groups as compared to 7±1 in the normal cortex. The size of vesicles was also enlarged, 4, 713±868 nm2 in permanent group and 3, 684±570 nm2 in temporary group as compared to 3, 491±507 nm2 in normal group.
The arteriole-venule in the ischemic cortex of temporary group also showed increased and enlarged pinocytotic vesicles, but no opening of tight junctions.
The results indicated that transcellular transport by pinocytotic vesicles plays an important role in the increase of capillary permeability observed in ischemic models of both groups. The vascular ultrasturctural differences between permanent and temporary groups were not statistically significant in either cortex.
