No abstract

Rupture of human cerebral arterial aneurysms is followed by prolonged cerebral arterial constriction; there is evidence that cerebrospinal fluid (CSF) from such patients contains vasoconstrictor substances which may cause the arterial constriction. The aim of this study was to develop a small animal model for investigating the effects of such CSF on the calibre of cerebral vessels in situ. Carotid angiography of the cerebral arteries of the rat visualizes the internal carotid, middle cerebral, anterior cerebral and stapedial arteries plus the vertebrobasilar system. Prostacyclin was injected during carotid catheterisation to prevent spontaneous and random occlusion of these cerebral arteries; in the presence of prostacyclin there was no arterial occlusion for up to 5 h. The resolution achieved by the angiographic technique, which magnified the cerebral circulations 2.9 times, was sufficient to measure the diameter of the internal carotid and stapedial arteries of the rat. Intracarotid infusion of 1.0 ml CSF collected from patients with ruptured cerebral arterial aneurysms caused a rapidly developing contraction of cerebral arteries lasting up to 5 h. Thus, we consider that the rat may also be used as a model for investigating the aetiology of human cerebral arterial constriction after aneurysmal rupture.

In nine baboons following intracisternal injection of a suspension of their own washed platelets, biphasic spasm was demonstrated by vertebral angiography. Constriction of the intra-arachnoid portion of the vertebral artery and the basilar artery was severe 10 minutes after the platelet injection, had begun to relax after one hour, but had returned on day 2 or 3. It persisted for about 8 days. The animals showed clinical evidence of neurological damage. At autopsy the vertebral and basilar arteries showed stripping of the endothelium, with adherent platelets, protein and other cells. There was blockage of some small branches. The brains showed ischaemic changes. The clinical phenomenon of spasm after subarachnoid haemorrhage was thus fairly closely modelled by the injection of platelets alone. There was some evidence that 5HT was probably not responsible for the delayed phase of spasm. Some suggestions are made about the mechanism.