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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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]

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