Abstract
The calcium entry blocker nimodipine is of potential interest for the prevention of neurologic damage in patients resuscitated after cardiopulmonary arrest [1]. Since nimodipine is rapidly and extensively distributed to the tissues and is efficiently extracted by the liver, the hemodynamic changes occurring after cardiopulmonary arrest and during cardiopulmonary resuscitation are likely to alter its pharmacokinetics, as described, for example, for lidocaine [2]. We therefore studied the pharmacokinetics of nimodipine after cardiopulmonary arrest in the dog.
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© 1991 Springer-Verlag Berlin Heidelberg
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Huyghens, L.P., Buylaert, W.A., Rosseel, M.T., Bogaert, M.G. (1991). Pharmacokinetics of Nimodipine in the Dog Resuscitated After Cardiopulmonary Arrest. In: Scriabine, A., Teasdale, G.M., Tettenborn, D., Young, W. (eds) Nimodipine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-48695-1_17
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DOI: https://doi.org/10.1007/978-3-642-48695-1_17
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-53405-1
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