Intimal Change following Subarachnoid Hemorrhage Resulting in Prolonged Arterial Luminal Narrowing

Abstract

The luminal surface of the cerebral arteries was examined by scanning electron micro scopy. Preliminary findings of the cases which succumbed to the aneurysmal rupture are reported with those obtained by light microscopic examinations of old autopsy specimens of the ruptured aneurysm.On SEM, the endothelial cells were lost on the luminal surface of the cerebral arteries and some were covered with fibrin meshwork confining red blood cells and other corpuscles.These findings were interpreted as endothelial injury with denudation of elastica and resulting mural thrombus formation.Light microscopic examination revealed that cerebral arteries which had had narrowing after SAH showed concentrically thickened intimal layer and the presence of rich vascularization partly in the subintimal layer. These histological pictures were interpreted as organized mural thrombus.Possible role which mural thrombosis plays in the pathogenesis of prolonged narrowing after SAH from the rupture of an aneurysm and its clinical significance, especially in connection with antifibrinolytic treatment, is discussed.

The Role of Arterioles and the Microcirculation in the Development of Vasospasm after Aneurysmal SAH

“…Reports on the action of these platelets and thrombi suggest that arteries are narrowed by mural thrombi as well as by proliferative organic changes in the arterial wall and such narrowing is often confused with prolonged vasospasm [62, 63]. Also, aggregated platelets may release vasoactive substances that produce smooth muscle constriction that results in arterial narrowing [60].…”

Localization and Alteration of Immunoreactive Endothelin-1 in Canine Basilar Arteries Following Subarachnoid Hemorrhage.

“…However, short-term arterial spasm has been difficult to document in humans after aneurysmal SAH [8], but angiographic vasospasm of the basilar artery was progressively greater and prolonged in dogs by successive injections of cisternal blood [31]. In addition, Someda et al [29] reported that endothelial injury in one-hemorrhage dogs occurred initially on day 2 or 3 and was followed by development of endothelial damage accompanied with vasospasm [16,29]. These results suggest that the onset and the severity of endothelial injuries in SAH rats may differ from those in dogs and humans after SAH, and endothelial injuries in dogs occurs initially on day 2 or 3, and progression of the damage is caused by continuous vasospasm after SAH.…”