An experimental study of ammonium intoxication.

摘要: Summary 1.In unanesthetized, normal dogs reversible ammonium intoxication was induced by intravenous infusion of (NH 4 ) 2 SO at varying rates and rapid injection CO 3 equivalent to 50 mg. (N) per kg. body weight. 2.A rise in blood urea nitrogen follows the ammonia nitrogen; pyruvic acid glucose levels are elevated; but no significant change α-ketoglutaric or plasma glutamine occurs. 3.Disodium α-ketoglutarate, L-arginine hydrochloride, monosodium glutamate, administered appropriate doses before, during, after induction intoxication, were ineffectual as protective agents. 4.The extent duration poisoning is shown be independent pH blood, affected salts employed, dependent upon dose rate administration. 5.From measurements made on constituents there evidence support thesis that symptoms derive from reductive amination acid, thus interrupting continuity tricarboxylic cycle necessary metabolism brain. 6.But it pointed out generally accepted do not necessarily reflect concentration these substances any particular moment organism a whole.