Nimodipine evoked dilation of cerebral arteries early during the development of late vasospasm in subarachnoid hemorrhage.

In subarachnoid hemorrhage (SAH) late cerebral ischemia may develop without significant visible narrowing of arteries at angiography, but in severe ischemic conditions "vasospasm" invariably seems to be present. The majority of patients with aneurysm rupture develop some degree of vasospasm, whereas relatively few suffer from ultimate brain infarction. The prophylactic use of the calcium antagonist Nimodipine is linked to a beneficial anti-ischemic effect in SAH, although narrowing of large bore arteries still seems to develop despite administration of this drug. Attenuation of vascular spasm, mainly in the arterioles has been implicated as the major mechanism of action, although a neuronprotective effect of Nimodipine has been suggested as well. The present paper presents fragmentary evidence that Nimodipine does elicit a vasoactive response in the cerebral vasculature early during the development of late cerebral vasospasm, and that this response seems closely linked to reversal of attendant ischemic symptoms.