Meptazinol (Wy 22811), a new analgesic: preliminary pharmacokinetic data.

The authors report on the pharmacokinetic profile of a new analgesic, meptazinol, from studies of plasma and urine levels after intravenous injection in 4 healthy volunteers. Conjugated product is formed very soon after injection and its concentration changes little over the period studied compared with the unchanged product where a fast, then a relatively slow phase of decline can easily be distinguished, suggesting a two compartment open system model. Meptazinol is predominantly eliminated in this conjugated form by urinary excretion of the metabolites.

The influence of imipramine on dopamine-induced ganglionic inhibition and neurogenic vasodilatation in the dog.

Imipramine potentiates the dopamine-induced inhibition in the paravertebral lumbar ganglia of the dog. Potentiation by imipramine of the dopamine-induced neurogenic vasodilatation in the isolated perfused gracilis muscle, is seen in cross-circulation preparations only, where imipramine is injected into the perfusion circuit of an isolated perfused gracilis muscle, it antagonizes the dopamine-induced neurogenic vasodilatation. When imipramine is injected intravenously into a dog with an autoperfused gracilis muscle, the peripheral antagonism masks the potentiating effect at the ganglionic level, and the dopamine-induced neurogenic vasodilatation is abolished.

Dopamine-induced neurogenic vasodilatation in isolated perfused muscle preparation of the dog.

Dopamine, injected into the lumbar aorta of the dog in doses which produce a reversible inhibition of synaptic transmission in the lumbar paravertebral ganglia (0.5-64x10-8 moles), produces a neurogenic vasodilatation in the isolated perfused hindleg or gracilis muscle. This was abolished by acute preganglionic decentralization and by administration into the perfused preparation of alpha-adrenoceptor blocking agents, but not of atropine or diphenhydramine.

Comparison of the therapeutic effectiveness of aprindine, procainamide and quinidine in chronic ventricular dysrhythmias.

1 A cross-over study with aprindine (100 mg daily after a loading dose of 200 mg), procainamide (4 × 1000 mg daily) and quinidine bisulphate (2 × 750 mg daily), all given orally, was performed in seventeen patients with stable chronic premature ventricular contractions following healed myocardial infarction. 2 The effectiveness of the treatment was evaluated during three consecutive weeks by continuous ambulatory tape recording of the electrocardiogram and repeated determinations of plasma levels were done. 3 The results showed that aprindine was more effective than procainamide and quinidine.