| Abstract: | Mice which were exposed to high concentrations of methylchloroform (1,1,1, trichloroethane) vapour died in cardiac fibrillation. Pretreatment 30 min. before the administration of methylchloroform gave the following antifibrillatory ED50's expressed in mg/kg intraperitoneally: β-adrenergic blocking agents: Propranolol: 1.7; (+)-propranolol: 45; (-)-propranolol 0.6; 1-(isopropylamino)-3-(o-phenoxyphenoxy)-2-propanol, HC1 (Ph QA 33): 6.5; 1-(isopropylamino)-3-(o-allylphenoxy)-2-propanol, HC1 (H 56/28 = aptin®): 19; 4-(2-isopropylamino-1-hydroxyethyl) methane sulphonanilide, HC1 (MJ 1999): 24; 2-(isopropylamino)-1-(p-nitrophenyl) ethanol, HC1 (INPEA): 50; dichloroisoprenaline (DCI): no effect; α-adrenergic blocking compounds: chlorpromazine: > 50; phenoxybenzamine, HC1 (dibenzyline®): no effect, phentolamine (regitin®): > 100. None of some commonly used antiarrhythmics: antazoline, HC1; lidocaine, HC1; phenytoin; procainamide, HC1 (pronestyl®) or quinidine sulphate had any effect. The most favourable therapeutic index (LD50/ED50) was found for (-)-propranolol ～ 200. The method appears particularly suitable for evaluation of compounds with antagonistic action on cardiac β-receptors and in this respect appears to be highly sensitive. |
