indication

For the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure

pharmacology

Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings.

mechanism of action

Dopamine is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings. In the brain, dopamine actas as an agonist to the five dopamine receptor subtypes (D!, D2, D3, D4, D5).

toxicity

LD₅₀ oral mice = 1460 mg/kg, LD₅₀ oral rats = 1780 mg/kg. Spasm or closing of eyelids, nausea, vomiting, cardiac arrhythmias, involuntary movements of the body including the face, tongue, arms, hand, head, and upper body; hypotension, haemolytic anaemia, urinary retention, duodenal ulcer, sialorrhea, ataxia, abdominal pain, dry mouth, nightmares, tachypnoea, bruxism, confusion, and insomnia.

biotransformation

Biotransformation of dopamine proceeds rapidly to yield the principal excretion products, 3-4-dihydroxy-phenylacetic acid (DOPAC) and 3-methoxy-4-hydroxy-phenylacetic acid (homovanillic acid, HVA).

absorption

Dopamine is rapidly absorbed from the small intestine.

half life

2 minutes

route of elimination

It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged.

drug interactions

Amitriptyline: The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect, dopamine.

Amoxapine: The tricyclic antidepressant, amoxapine, increases the sympathomimetic effect of dopamine.

Clomipramine: The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of dopamine.

Desipramine: The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of dopamine.

Doxepin: The tricyclic antidepressant, doxepin, increases the sympathomimetic effect of dopamine.

Entacapone: Entacapone increases the effect and toxicity of the sympathomimetic, dopamine.

Fosphenytoin: Risk of severe hypotension

Guanethidine: Dopamine may decrease the effect of guanethidine.

Imipramine: The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of dopamine.

Isocarboxazid: Increased arterial pressure

Linezolid: Possible increase of arterial pressure

Methyldopa: Increased arterial pressure

Midodrine: Increased arterial pressure

Moclobemide: Moclobemide increases the sympathomimetic effect of dopamine.

Nortriptyline: The tricyclic antidepressant, nortriptyline, increases the sympathomimetic effect of dopamine.

Phenelzine: Increased arterial pressure

Phenytoin: Risk of severe hypotension

Rasagiline: Increased arterial pressure

Reserpine: Increased arterial pressure