• E Vinge, L Brandt, B Ljunggren, and K E Andersson.
• Department of Clinical Pharmacology, University Hospital, Lund, Sweden.
• Stroke. 1988 May 1;19(5):644-7.

AbstractTwenty-four patients with subarachnoid hemorrhage due to rupture of a supratentorial aneurysm underwent surgery within 72 hours after subarachnoid hemorrhage. Immediately after clipping of the aneurysm the patients were treated with intravenous nimodipine for at least 7 days and then received the drug orally for another week. Nine patients had a documented or probable intake of aspirin or other nonsteroid anti-inflammatory drug during the days preceding admission. In all patients there was a gradual increase in serum thromboxane B2 concentration from low to normal levels during the treatment period, the increase being most pronounced in patients with prior nonsteroid anti-inflammatory drug intake. Thromboxane B2 concentrations were similar to those of four control patients not receiving nimodipine. In three patients who developed delayed ischemic dysfunction despite "therapeutic" nimodipine plasma concentrations, the thromboxane B2 levels were low or normal. Our present results do not support the idea that nimodipine exerts an effect on platelet function in patients with aneurysmal subarachnoid hemorrhage.

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