Beta adrenergic receptors and glucagon in seizures from exposure to oxygen at high pressure (OHP).
Previous studies have shown that sympathetic factors and blood glucose are of importance in the development of seizures and lung damage from OHP. In the present study we examined the influence of beta sympathetic agonists and blocking agents and glucagon on OHP toxicity. Rats were exposed to 6 ATA OHP and examined for time-to-seizure and lung damage. Pretreatment with propranolol increased the time-to-seizure by 70% and practolol by 50% without altering gross lung appearance or lung wet wt/dry wt. Propranolol and practolol also prevented brain glycogen depletion prior to seizure which otherwise occurred in subconvulsive exposure to OHP. Isoproterenol and glucagon pretreatment had no effect on time-to-seizure but isoproterenol did increase lung injury. Both practolol and propranolol block the beta-receptor influence on adenyl cyclase-stimulated second messenger production, while both isoproterenol and glucagon activate adenyl cyclase to produce second messenger. Our results may suggest a possible role for second messenger in mediating some of the acute toxic effects of OHP on the CNS.
D000818:Animals; D005934:Glucagon / Q000494:pharmacology*; D006931:Hyperbaric Oxygenation; D007545:Isoproterenol / Q000494:pharmacology; D008168:Lung / Q000473:pathology; D008297:Male; D011217:Practolol / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D012640:Seizures / Q000209:etiology / Q000378:metabolism* / Q000473:pathology
D011943:Receptors, Adrenergic, beta; D005934:Glucagon; D011433:Propranolol; D007545:Isoproterenol; D011217:Practolol