The chapters in this volume are based on presentations made at the Second International Symposium on Nimodipine held in Miami Beach, Florida, USA, on April 25 -28, 1990. The Symposium dealt primarily with the results of recent clinical studies on the effects of nimodipine in acute neurological disor ders: subarachnoid hemorrhage, acute ischemic stroke, cerebral resuscitation following cardiac arrest and head trauma. The first session was devoted to pharmacology of nimodipine and its effects in various models of cerebral ischemia. Nimodipine was synthesized at the Research Laboratories of Bayer AG, Wuppertal, Germany, by Meyer et al.; its pharmacology was studied initially by Hoffmeister, Kazda, Garthoffand Towart, also in Wuppertal. Nimodipine was found to be a potent cerebral vasodilator and to reduce mortality in stroke-prone spontaneously hypertensive rats. In addition to its cerebrovascu lar effects, nimodipine was shown to block L-type Ca2+ channels in neurons, to reduce neuronal uptake of Ca2+ and to antagonize various neurotoxins. The beneficial effects of nimodipine in the treatment of disorders of central nervous system may be attributed either to cerebrovascular or to a direct neuronal action with evidence favoring increasingly the latter mechanism.
The chapters in this volume are based on presentations made at the Second International Symposium on Nimodipine held in Miami Beach, Florida, USA, on April 25 -28, 1990. The Symposium dealt primarily with the results of recent clinical studies on the effects of nimodipine in acute neurological disor ders: subarachnoid hemorrhage, acute ischemic stroke, cerebral resuscitation following cardiac arrest and head trauma. The first session was devoted to pharmacology of nimodipine and its effects in various models of cerebral ischemia. Nimodipine was synthesized at the Research Laboratories of Bayer AG, Wuppertal, Germany, by Meyer et al.; its pharmacology was studied initially by Hoffmeister, Kazda, Garthoffand Towart, also in Wuppertal. Nimodipine was found to be a potent cerebral vasodilator and to reduce mortality in stroke-prone spontaneously hypertensive rats. In addition to its cerebrovascu lar effects, nimodipine was shown to block L-type Ca2+ channels in neurons, to reduce neuronal uptake of Ca2+ and to antagonize various neurotoxins. The beneficial effects of nimodipine in the treatment of disorders of central nervous system may be attributed either to cerebrovascular or to a direct neuronal action with evidence favoring increasingly the latter mechanism.
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