effect of different lipophyllic beta-blockers on the minimal electro-shock seizure threshold [MEST] in mice

The effect of different beta-blockers on the minimal electro-shock seizure threshold [MEST] in mice, an index of generalized seizure susceptibility, was studied. Equipolent doses of the lipophilic beta-adrenergic blockers propranolol, pindolol,.oxprenolol and metoprolol significantly reduced the MEST after acute or chronic use [P < 0.05], however, this reduction was not significantly dose-dependant or significantly different between them. These drugs also antagonised the effect of beta agonists sulbutamol and isoprenaline, as well as that of the antiepileptic drugs phenytoin, valproate and clonazepam in elevating the seizure threshold. No significant change in blood glucose level or brain GABA content accompanied these acute or chronic effects on MEST, except for propranolol. It is concluded that lipophylic beta-adrenergic blockers enhanced seizure susceptibility mainly by blocking beta-adrenoceptors in brain. The magnitude of. this effect does not seem to be significantly altered by the selectivity of the beta block or by the possession of partial agonist activity by some of these drugs

comparative study of clondine and bromocrytine on growth in some growth-retarded children

Children with short stature, but otherwise healthy, and showing a subnormal GH [growth hormone] release to insulin hypoglycemia were evaluated for growth after 3 months of treatment with each of placebo [multivitamin tablet b.i.d.], Clonidine [b.i.d.] or bromocryptine 2.5 mg/d nocte], consecutively. Clonidine significantly increased OH release in these dwarfs, and this was associated with significant increase in height 3 months after treatment Bromocryptine had a mild enhancing effect on linear growth and plasma Gil level, while placebo had no significant effect. It is suggested that clonidine, probably acting centrally to augment hypothothalamic GHRH secretion and consequently GM release, might be more useful agent than bromocryptine in such growth retarded children. The results also suggest that alpha 2-adrenergic dysfunction in hpothalmus is more involved than a dopaminergic disorder 4 disturbing GM release from anterior pituitry with subsequent retardation of growth

study on the effect of propranolol on seizure threshold in mice: its possible mechanisms and interaction

The effect of propranolol on the minimal electroshock seizure threshold [MEST] in mice, an index of generalised seizure susceptibility, was studied This lipophylic, non-selective beta-adrenergic blocker reduced the MEST after acute or chronic use [P < 0.01]; it also antagonised the effect of the beta-adrenergic agonists isoprenaline and salbutamol as well as that of the anti-epileptic agents phenytoin, valproate, and clonazepam in elevating the MEST. These acute or chronic effects were not accompanied by any significant hypoglycaemia, but the chronic effect was associated with a significant reduction in brain GABA content [P <0.01]. Hepatic microsomal enzyme induction with rifamycin effectively blocked the chronic effect of the drug in reducing the MEST. It is concluded that the effect of propranolol in enhancing seizure susceptibility is due the parent compound and is mainly mediated by blocking central beta-adreno ceptors; reduction in brain GABA might be implicated in the chronic effect of this drug. It is possible that this drug could aggravate or disturb the control of generalized epilepsy in man