• P A Calle, M G Bogaert, L De Ridder, and W A Buylaert.
• Heymans Institute of Pharmacology, Gent, Belgium.
• Naunyn Schmiedebergs Arch. Pharmacol. 1990 Jun 1;341(6):586-91.

AbstractBrain damage after resuscitation from cardiac arrest is believed to be related to calcium influx in ischaemic neurons and to postischaemic calcium-dependent vasospasm. We therefore evaluated the potentially protective effects of the calcium-entry blocker nimodipine in a cardiopulmonary arrest model in the rat. Male Wistar rats were anaesthetized with ketamine (group I) or hexobarbital (group II) and subjected to a KCl-induced cardiac arrest during 7 min (group I) or 12 min (group II). Five minutes after resuscitation, the rats were treated intravenously in a randomized and blind fashion. Group I received either saline or 1 microgram.kg-1.min-1 or 5 micrograms.kg-1.min-1 of nimodipine and group II either saline or 1 microgram.kg-1.min-1 of nimodipine. Survival, occurrence of seizures and neurological status were assessed daily during 7 days after resuscitation. On day 7, the brains of the surviving rats were perfusion-fixed and a histopathological evaluation of the hippocampus was performed. Nimodipine, in the doses tested, had no beneficial influence on the 7 day survival rate, nor on the occurrence of seizures and the neurological and histopathological scores in the rats surviving after 7 days. With the highest dose of nimodipine, there was even a trend towards a decrease of the survival rate, probably related to the drug's hypotensive effect. Therefore, our data do not show a protective effect of nimodipine after cardiac arrest.

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