Preventive nimodipine and acute aneurysm surgery. Heading for the control of complications after aneurysmal subarachnoid hemorrhage.
Experimental and clinical studies have been performed to investigate the validity of a pharmacological approach to prevent delayed ischemic neurologic deficit from vasospasm after subarachnoid hemorrhage: the calcium channel blocker nimodipine was administered intravenously and perivascularly. Pial arteries of cat dilated by 25% during 1 microgram/kg-1 min-1 intravenous infusion; perivascular application of a 2.4 X 10(-5) M solution induced a 21% dilatation, the ethanol-containing solvent alone a 6% dilatation. A 1 microgram/kg-1 min-1 intravenous infusion of nimodipine in patients during EC-IC bypass operation led to a 16% dilatation of pial arteries; the solvent remained without effect. Perivascular application of a 2.4 X 10(-5) M solution during aneurysm surgery evoked a 70-80% dilatation of pial arteries, solvent-treated arteries dilated between 5 and 40%. In a multicenter study on 120 patients with preventive nimodipine treatment and acute operation of ruptured aneurysms, the incidence of delayed cerebral ischemia and fixed neurologic deficit was 1.7%. It is concluded that acute surgery of ruptured cerebral aneurysms and treatment with the calcium antagonist nimodipine substantially reduce the risk of symptomatic vasospasm.[1]References
- Preventive nimodipine and acute aneurysm surgery. Heading for the control of complications after aneurysmal subarachnoid hemorrhage. Auer, L.M. Neurochirurgia. (1985) [Pubmed]
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