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Updated: Feb 9, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
[EVALUATION OF NEUROPROTECTIVE ACTIVITY OF COMPLEX IMPACT OF MAGNESIUM OF SULFATE, LAMOTRYGINE AND N-ACETYLCYSTEINE
M Samsonia1, M Kandelaki1, N Baratashvili1
11A. Tsereteli Kutaisi State University, Department Of Pharmacy; 2Pharmaceutical Company - Legion "Provisus", Kutaisi, Georgia.
Abstract:
Cerebrovascular diseases of ischemic origin still remain the leading cause of death and disability of the population. In acute cerebral discirculation conditions, anaerobic glycolysis is activated, ATP formation rate decreases, the ion pumps work is disrupted and superoxide radicals are formed. Eventually, ionic asymmetry leads to the cytotoxic and vasogenic brain edema. Therefore, it is extremely important to induce simultaneous (complex) effect of medications on the key mechanisms of neuronal damage in process of survival of brain cells during acute ischemic stroke. On this evidence, in the experiments on rats (n=70), the neuroprotective activity of magnesium sulfate, lamotrigine and acetylcysteine as a combination was studied, under normobaric hypoxia conditions (after carotid ligation of the right carotid artery). Researches have shown the use of magnesium sulfate (1000 mg/kg, ip), lamotrigine (20 mg/kg, per os) and acetylcysteine (200 mg/kg, per os) as a combination, is accompanied by increasing antioxidant and neuroprotective activity of drugs. The protective index in this group was 2.18 and the differences were statistically significant compared to control group (p<0.05). All factors - enhancement of the antioxidant systems of neurons by acetylcysteine, inhibition of glutamate excitotoxicity by lamotrigine and correction of ion stress by magnesium ions, critically increase the time prior to apnea. Accordingly, the combination of magnesium sulfate, lamotrigine and acetylcysteine is able to protect brain cells from the damaging effects of oxygen-glucose deprivation and can be effectively used for pharmacological correction of hypoxic brain damage (in acute ischemic stroke).
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