Pathogenesis of état criblé in experimental hypertensive rats

Abstract The pathogenesis of etat crible in experimental hypertensive rat brain was studied. Macroscopically, the hypertensive rat brain showed marked subarachnoidal edema. Cystic dilatation of the subarachnoid space, softening, and perivascular dilatation or etat crible, in the caudate putamen, frontoparietal cortex, and basal ganglia were observed by light microscope. Perivascular dilatation was noted not only around the intracerebral arteries and arterioles but also around the veins and venules. Transmission and scanning electron microscopy also confirmed the presence of perivascular dilatation around the same vessels. In addition, transmission electron microscopy confirmed the increased permeability of the endothelial cells in the intracerebral arteries, arterioles, veins, venules, and capillaries of brains with etat crible. Severe medial cell injuries of the arteries and arterioles and edema-induced destruction of the brain around the dilated perivascular space were also observed. Scanning electron microscopy revealed mild or cystic dilatation of the perivascular space, a net-like structure on both sides of the arachnoidal cells resulting in markedly dilated and numerically increased fenestra, and degenerative changes in the perivascular brain tissue. In conclusion, etat crible in experimental hypertensive rat brain results from an increase in perivascular fluid-induced degeneration of the perivascular brain tissue that is in turn induced by an increase in the permeability of blood vessels. Copyright © 2001 by National Stroke Association