1. Coronary ligatjon (CL) in dogs produced ventricular fibrillation (VF) in 80% animals, myocardial glycogenolysis and increased cholinesterase (ChE) activity of myocardium and blood. 2. Pretreatment with morphine sulphate significantly reduced the incidence of CL-induced VF and prevented the biochemical changes induced by ischaemia. 3. Pretreatment with atropine methiodide or bilateral vagotomy failed to affect the incidence of CL-induced VF significantly, but increased the ischaemiai-induced depletion of the ventricular myocardial glycogen content. 4. The results indicated that neither genesis nor prevention of VF followi'ng myocardial ischaemia (MI) were related to the haemodynamic and biochemical changes in the myocardium. 5. The anti-arrhythmic activity of narcotic analgesics are probably due to their central actions. 6. The central nervous system and the adrenergic system seem to play important role in the genesis of post-ischaemic arrhythmias, while the cholinergic system appears to have a cardio-protective action.

1. At low doses, dopamine agonists, apomorphine (0.25-0.5 mg/kg), lisuride (0.001-0.01 mg/kg) and pergolide (0.005-0.01 mg/kg) lowered the latency period of haloperidol (0.25 mg/kg) induced catalepsy in rats. However, when higher doses were given, apomorphine (5.0-10.0 mg/kg) lisuride (0.05-0.1 mg/kg) and pergolide (0.25-1.0 mg/kg) increased the latency period. 2. Pretreatment with low doses of haloperidol(0.025-0.05mg/kg) partially prevented the lowering of the latency period due to low doses of dopamine agonists. 3. These findings tend to provide one more evidence to confirm that more than one group of dopamine receptors are involved in this typical biphasic response.

1. Two newly synthesised sulfonium analogs have been tested for their dopamine agonist activity using biochemical methods. 2. Addition of dopamine and the analogs caused an increase in cyclic AMPproduction in a dose dependent manner in rat striatal slices. 3. Fluphenazine the dopamine antagonist when added to the incubation medium inhibited the increase in cyclic AMP levels produced by dopamine and the analogs. 4. Dopamine and apomorphine, the known agonists produced inhibition of 3H -ADTN binding to rat brain homogenates. Both the slufonium analogs also produced, inhibition of 3H - ADTN binding to rat brain homogenates. 5. The IC50 values of these two analogs (6.5 uM and 2uM) were higher than that of dopamine (188nM) and apomorphine (20nM).