Because the dopamine metabolized with the participation of MAO, inhibition of this enzyme leads to prolongation and potentiation of the effect of dopamine. Patients who receive or have received MAO inhibitors during the previous 2-3 weeks should be given a significantly lower dose of dopamine (the initial dose should be 1/10 of the usual dose).
The simultaneous administration of dopamine and diuretics can be accompanied by an additive and potentiating effect.
When used simultaneously with cyclopropane or halogenated hydrocarbons for inhalation anesthesia, the risk of arrhythmia increases (extreme caution should be observed). The introduction of dopamine against the background of tricyclic antidepressants leads to an increase in its effects (possibly developmentarrhythmia, severe arterial hypertension).
Beta-blockers (propranolol and metoprolol) are antagonists of dopamine cardiac effects. Butyrophenones (including haloperidol) and phenothiazines can reduce the effect of dopamine.
Alkaloids of ergot, oxytocin increase the vasoconstrictor effect of dopamine, which is accompanied by the danger of ischemia and gangrene, as well as severe arterial hypertension.
Joint application with phenytoin promotes the development of arterial hypotension and bradycardia.
With simultaneous administration with guanethidine, octadine, sympathomimetic action is enhanced.
Other sympathomimetics, as well as cocaine intensify cardiotoxic action.
With simultaneous use with levodopa, the risk of arrhythmias increases.
At simultaneous application with hormones of a thyroid gland probably amplification of action both dopamine, and hormones of a thyroid gland.
Ergometrine, ergotamine, methylergomethrin, oxytocin increase the vasoconstrictor effect and the risk of occurrence of ischemia and gangrene, as well as severe arterial hypertension, up to intracranial hemorrhage.
With simultaneous use with cardiac glycosides, an increased risk of cardiac arrhythmias, an additive positive inotropic effect, is possible.
Reduces the antianginal effect of nitrates, which in turn can reduce the pressor effect of sympathomimetics and increase the risk of arterial hypotension.
Pharmaceutically incompatible with alkaline solutions (inactivate dopamine), oxidants, iron salts, thiamine (promotes the destruction of vitamin B1).