Ipratropium pharmacokinetics and molecular data

Pharmacokinetics
Mechanism of action Absorption Metabolism Distribution Elimination

Mechanism of action
Ipratropium bromide is an anticholinergic (parasympatholytic) agent which, based on animal studies, appears to inhibit vagally mediated reflexes by antagonizing the action of acetylcholine, the transmitter agent released from the vagus nerve. Anticholinergics prevent the increases in intracellular concentration of cyclic guanosine monophosphate (cyclic GMP) which are caused by interaction of acetylcholine with the muscarinic receptor on bronchial smooth muscle. Return to top

Absorption
The bronchodilation following inhalation of ipratropium bromide is primarily a local, site-specific effect, not a systemic one. Much of an administered dose is swallowed, but not absorbed, as shown by fecal excretion studies. Following nebulization of a 2 mg dose, a mean 7% of the dose was absorbed into the systemic circulation either from the surface of the lung or from the gastrointestinal tract. Return to top

Metabolism
Ipratropium bromide is partially metabolized. Return to top

Distribution
Ipratropium bromide is minimally bound (0 to 9% in vitro) to plasma albumin and α1-acid glycoprotein. Return to top

Elimination
The half life of elimination is about 1.6 hours after intravenous administration. Autoradiographic studies in rats have shown that ipratropium bromide does not penetrate the blood-brain barrier. Return to top