| pubmed-article:7198471 | pubmed:abstractText | In anesthetized dogs, (+)-(R)-alpha ((S)-1-[(3,3-di-3-thienylallyl)amino]-ethyl)-benzylalcohol hydrochloride (tinofedrine hydrochloride, D 8955) causes a remarkable increase of cardiac output by positive inotropic and chronotropic stimulation of the heart and simultaneous reduction of peripheral vascular resistance. The effect is antagonized by beta-adrenergic blocking drugs. In comparison with typical beta-agonists (e.g., orciprenaline) tinofedrine at inotropically equieffective doses, has a much weaker effect on the heart rate. Measurement of tissue blood flow by radioactive tracer microspheres after tinofedrine exhibited a rather homogeneous increased perfusion in all parts of the brain, as well as myocardium, kidneys and liver. In coronary circulation tinofedrine causes vasodilation so that in a therapeutic dose range increased work load is equalized by a sufficient myocardial supply. Tinofedrine itself neither caused a disturbance of heart rhythm nor worsened aconitine-induced arrhythmias in anesthetized rats. Simultaneous application of digoxin or diazepam did not influence the action of tinofedrine; there was no evidence of any incompatibility of such combinations. Experiments with a possible metabolite (l-norephedrine) showed that it is not involved in the action of tinofedrine. | lld:pubmed |
