Abstract
Forty adult cats were subjected to this study in order to examine the changes in permeability of major cerebral arteries after subarachnoid hemorrhage by using three kinds of tracers with varied molecular sizes.
Experimental cerebral vasospasm was produced in 25 cats. Three days after intracisternal injection of 3 ml of autologous blood, the basilar artery was exposed by transclival approach, then continuously irrigated with the mixture of blood and CSF for 4 hours. After gross vasospams in the basilar artery was seen, the three tracers, HRP (horseradish peroxidase), NF (native ferritin), CG (colloidal gold, 5 nm and 20 nm particle size), were administered through the subclavian artery. The basilar artery was examined under transmission electron microscopy. Tracer study was also performed in 15 normal animals.
In the basilar artery contracting for 4 hours, endothelial cells were deformed along the corrugated internal elastic lamina, and smooth muscle cells were distorted. HRP reactive products and NF were observed in the endothelial plasmalemmal vesicles, interendothelial spaces, subendothelial spaces, and widened intercellular spaces in smooth muscle layer. However, CG was not observed in the vessel wall. Most noticeable routes to the smooth muscle layer appeared to be interendothelial spaces with broken tight junctions following subarachnoid hemorrhage. In the normal basilar artery, no tracer was observed in the vessel wall, although HRP reactive products filled some plasmalemmal vesicles of endothelial cells.
These results suggests that intraluminal vasoactive substances, with smaller molecular sizes than NF, may penetrate the vessel wall of major cerebral arteries in the early stage of subarachnoid hemorrhage, resulting in the progressing and long-lasting vasospasm in the major cerebral arteries. These permeability changes of major cerebral arteries may play an important role in the pathogenesis of cerebral vasospasm.
