Ultrastructural changes of the basilar artery following experimental subarachnoid haemorrhage. A morphological study on the pathogenesis of delayed cerebral vasospasm.

Recent experimental studies have shown, that the endothelium of cerebral vessels undergoes significant changes after subarachnoid haemorrhage which may lead to biochemical changes at the endothelial surface with disturbance of the delicate homeostasis of vasodilating and vasoconstricting mechanisms which are thought to be responsible for preservation of the tones of the cerebral vasculature. Ultrastructural studies incorporating different forms of microscopic observations of the endothelium after SAH representing a prerequisite for further investigations on the pathogenesis of cerebral vasospasm are scarce. The experimental study was performed in order to investigate and define more precisely the pathomorphological changes at the endothelial surface of the basilar artery of dogs after experimental SAH. Two separate injections of autologous blood into the cisterna magna within 72 hours resulted in extensive angiographic narrowing of the diameter of the basilar artery of all animals. Histological studies of the basilar artery including light microscopic, transmission electron microscopic, scanning electron microscopic and freeze cracking microscopic examinations demonstrated severe pathomorphological changes at the endothelial surface. These consisted mainly of infolding and corrugation of the endothelium, disorientation and desquamation of endothelial cells as well as of vacuolation and ingrowth of fibrous tissue between the endothelial and muscular layer. No pathomorphological changes could be observed in the muscular layer. As the described post-haemorrhagic ultrastructural changes of the endothelium cerebral vessels in spasm are likely to represent the morphological basis of the delayed form of cerebral vasospasm future research on its pathogenesis should primarily focus on the structural and biochemical taking place at the endothelial surface of the cerebral vasculature after SAH.