Cerebral cortical changes in acute experimental hypertension: An ultrastructural study.

Multiple focal cortical areas of increased vascular permeability to tracer substances occur in experimental hypertensive encephalopathy. In this study, rats with angiotensin-induced acute hypertension were used to determine whether increased permeability was associated with focal cerebral edema and if so, the tissue component involved. In addition, the mechanism of increased permeability and the types of vessels involved were investigated using horseradish peroxidase as a tracer. Quantitative morphometric studies 8 minutes after the onset of hypertension demonstrated significant perivascular glial swelling around arterioles, venules, and capillaries; the swelling was confirmed to the permeable areas and absent in the nonpermeable areas of the same animals. Ninety seconds after the onset of hypertension, horseradish peroxidase reaction product was present in focal superficial segments of the walls of penetrating arterioles but rarely in venular and capillary walls. At this time period endothelial cells showed prominent pinocytotic uptake of tracer. Eight minutes after the onset of hypertension, reaction product was again found in arteriolar walls and had extravasated into the surrounding extracellular space of the neuropil as well. Extravasation also occurred through capillary and venular walls but was less frequent. At this time interval endothelial pinocytotic activity was still prominent. There was no mechanical damage of vessel walls in the form of endothelial discontinuities or disruption of interendothelial spaces. Tracer was not found in interendothelial jundtions in continuity from lumen to base. The principle mechanism of increased permeability was enhanced pinocytosis, which occurred rapidly, being demonstrable 90 seconds after the onset of hypertension; it was observed principally in permeable arteriolar segments.