Abstract
Rat cerebral vessels in ischemic lesions, introduced by plugging a silicon rubber cylinder into the terminal segment of the unilateral internal carotid artery, were investigated under an electron microscopy, immediately after either ischemic period or recirculation-period following ischemia. Recirculation into ischemic lesion was achieved by pulling the cylinder out from the artery.
The denudation of endothelial cells from the basement membrane was observed in the small arteries of animals having persistent ischemia for more than 6 hours. On the contrary, in a recirculation group with occlusion for 2 hours was enough for occurring endothelial denudation of the artery in ischemic lesions, if it received recirculation for 2 hours.
Ultrastructural changes of medial smooth muscle cells in the arteries, such as swelling and destruction of mitochondrial cristae and cytoplasmic swelling leading to disappearance of contractile cytoplasmic filaments, preceeded endothelial denudation. Accordingly, medial smooth muslce cells seemed to be more vulnerable against ischemia than endothelial cells.
Endothelial denudation surely exacerbated vascular changes so that medial necrosis appeared to be accomplished beneath the denuded areas and erythrocytes, platelets and carbon particles were allowed to be leaked into the media from the lumen to permeate into cytoplasmas of smooth muscle cells. Contrary to arteries, veins in the infarcted areas did not show endothelial denudation nor medial necrosis. As duration of occlusion was longer, arterial lesions were more intense resulting in more marked increase of vascular permeability.
