Study of the protection on afforded by nicergoline against the effects of cerebral ischemia in the cat.

  • 1 March 1975
    • journal article
    • research article
    • Vol. 25  (3) , 410-3
Abstract
The cortical evoked potential of the two cerebral hemispheres of the cat is taken as the parameter of brain function; its course is studied during strangulation which determines its disappearance, and especially during strangulation release (recovery phase). Under these experimental conditions, the injection of 9% NaCl solution in each carotid does not modify the symmetry of recovery in the two cerebral hemispheres. The unilateral injection of increasing doses of 1,6-dimethyl-8beta-(5-bromonicotinoyl-oxymethyl)-10alpha-methoxyergoline tartrate (nicergoline) (20 to 400 mug) produces more rapid recovery on the treated side. This is also the case for the unilateral injection of 40 mg of sodium malonate. Observation of this effect in the hypoventilated, hypercapnic animal, with an already dilated cerebral network suggests that the mechanism of the protection afforded is not due to vasodilatation of the cerebral network produced by either of the two products. The effect of nicergoline disappears when a previous i.v. injection of sodium malonate has inhibited anoxic depolarization of the cellular membrane and inhibited the fall in cerebral ATP caused by ischemia. It would thus appear that the anti-ischemic properties of nicergoline, acting at the level of the central nervous system, are due to an effect on the cellular membrane or to an inhibiting effect on the metabolism of the brain cell. Supplementary experiments, involving the use of more specific pharmacological reagents should allow its action to be localized at the level of the membrane and/or of cellular metabolism.

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