Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feinberg, W. M.
Right arrow Articles by Bruck, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feinberg, W. M.
Right arrow Articles by Bruck, D. C.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH

Stroke, Vol 24, 10-13, Copyright © 1993 by American Heart Association


ARTICLES

Effect of oral nimodipine on platelet function

WM Feinberg and DC Bruck
Department of Neurology, Arizona Health Sciences Center, Tucson 85724.

BACKGROUND AND PURPOSE: Nimodipine, a calcium antagonist, has been reported to have beneficial effects in acute ischemic infarction. Some calcium channel antagonists have antiplatelet effects. We investigated the effect of oral nimodipine on platelet function in healthy volunteers. METHODS: Twelve healthy volunteers (6 men and 6 women, mean age 32.9 +/- 5.6 years) took 30 mg nimodipine every 6 hours for 24 hours, followed by a week with no medication, followed by 60 mg every 6 hours for 24 hours. Ex vivo platelet function was measured at baseline, 1 hour after the first dose at each dosage strength, and 1 hour after the last dose at each dosage. Platelet studies included aggregation and adenosine triphosphate release in response to collagen, epinephrine, and adenosine diphosphate; maximal rate of primary aggregation; threshold adenosine diphosphate concentration for second-phase aggregation; and thromboxane B2 release at threshold aggregation. The bleeding time was measured at baseline and after the last 60-mg dose of nimodipine. RESULTS: No change in any platelet function study was seen with 30 mg nimodipine every 6 hours. Platelet function studies were also unchanged after 60 mg every 6 hours, except for a slight decrease in aggregation and adenosine triphosphate release in response to suprathreshold (10 microM) adenosine diphosphate (p = 0.001, Student's paired t test). There was no significant change in bleeding times. CONCLUSIONS: Oral nimodipine has minimal antiplatelet activity in young, healthy subjects.


This article has been cited by other articles:


Home page
Canadian J. AnesthesiaHome page
T Nishiyama, T Yokoyama, T Matsukawa, and K Hanaoka
Continuous nicardipine infusion to control blood pressure after evacuation of acute cerebral hemorrhage
Can J Anesth, December 1, 2000; 47(12): 1196 - 1201.
[Abstract]


Home page
StrokeHome page
C. Legault, C. D. Furberg, L. E. Wagenknecht, A. T. Rogers, D. A. Stump, L. Coker, B. T. Troost, and J. W. Hammon
Nimodipine Neuroprotection in Cardiac Valve Replacement : Report of an Early Terminated Trial
Stroke, April 1, 1996; 27(4): 593 - 598.
[Abstract] [Full Text]