Dopamine

[PHW2:p194-196]

=== Unfinished ===

(Quick note only)

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In certain cells in brain and interneurons of the autonomic ganglia, dopamine is released as a neurotransmitter and is not converted to NE

Pharmacodynamics

Acts on alpha, beta adrenergic receptors, as well as dopamine (D1 and D2) receptors
* D1 = Gs coupled
* D2 = Gi coupled

CVS

At lower rate of infusion

Beta1 effect dominate

Increased contractility, heart, CO, and coronary blood flow

Also stimulates release of endogenous NE

At higher rate of infusion

Alpha effect dominate

Increased SVR and venous return

Increased pulmonary vascular resistance

NB:

Less pro-arrhythmic than adrenaline

Extravasation can cause tissue necrosis

Respiratory

Attenuation of carotid body response to hypoxaemia

Splanchnic

Vasodilate mesenteric vessels
* Via D1 receptors

Improved urine output, due to
* ?Increased renal perfusion
* Inhibition of proximal tubular Na+ resorption
* Improved CO, BP

CNS

Dopamine does NOT cross BBB
* Precursor L-dopa does

But in CNS, dopamine causes
* Extrapyramidal movement
* Inhibition of prolactin secretion

Others

Stimulation of chemoreceptor trigger zone
--> N&V

Increased gastric transit time
* i.e. decreased gastric emptying

Interaction

Effects of dopamine may be increased or prolonged in patients using MAO inhibitors

Only administered IV
* Preferably via a central vein

Onset of action 5 min

Duration of action 10 min

Halflife = 3 min

Metabolism
* By MAO and COMT in the liver, kidney, and plasma

Metabolites
* 3,4-dihydroxyphenylacetic acid
* Homovanillic acid (HVA)

Metabolites are excreted in urine as conjugates

25% of the administered dose of dopamine is converted to NE in the sympathetic nerve terminals

200 or 800 mg in 5 mL

Preservative = Sodium metabisulphite

Used to improve haemodynamics and urine output