[Experimental cerebral infarction in the dog. Ultrastructural study of capillary permeability by freeze-fracture replica].

  Underlying mechanisms which lead to brain edema following ischemic insults have been subjects of much debate. In this study, experimental cerebral infarction was produced in dogs by injecting one or two silicone rubber cylinders through the cervical internal carotid artery. Twenty-four hours after embolization, animals were killed and morphometrical analyses in the capillary endothelial cell membranes in the cortex were done by freeze-fracture replica in addition to conventional ultra-thin section using the transmission electron microscope.   In ultra-thin sections of capillary endothelium in the ischemic cerebral cortex, surface infolding and increase in number of pinocytotic vesicles were recognized, but no findings of opening of tight junction were ascertained.   In freeze-fracture replicas of capillary endothelium of both normal and ischemic cerebral cortex, tight junction was presented as the network of ridges composed of about 100 Å particles on the protoplasmic face (PF) and grooves on the extracellular face (EF). In the ischemic cortex, arrange ment of strands of these protein particles was not changed. In replica preparations, too, no definite findings of opening junction were certificated. Pinocytotic vesicles were seen as invaginations on the PF and as protrusions on the EF. In the ischemic cortex, the average number per square μm was in creased. On the luminal front, it reached to 22.0 (on the PF) and 29.5 (on the EF) as compared to 7.2 and 9.0 in the normal cortex, respectively. The size of vesicles was also enlarged; 4,990.7± 798 nm2 (on the PF) and 4,762.8±878 nm2 (on the EF) as compared to 3,567.7±570 nm2 and 3,404.5±573 nm2 in the normal cortex, respectively.   These results indicate that transcellular transport by pinocytotic vesicles has an important role in increase of capillary permeability observed in an ischemic model.