ry, bronchial, and sweat glands. Next are the receptors in the eye and heart, followed by the receptors in the GI tract.
The principal clinical effects of atropine are a reduction in salivary, bronchial, and sweat gland secretions; mydriasis; cycloplegia; changes in heart rate; contraction of the bladder detrusor muscle and of the GI smooth muscle; decreased gastric secretion; and decreased GI motility. At lower doses, a paradoxical decrease in heart rate occurs, and at higher doses, effects are seen at nicotinic receptors in autonomic ganglia, causing restlessness, hallucinations, disorientation, and/or delirium. Unlike scopolamine, atropine does not produce CNS depression (drowsiness, euphoria, amnesia, fatigue, decreased REM sleep) at usual therapeutic doses. Also, atropine's antimuscarinic potency is greater in the heart, bronchial, and GI smooth muscle, and is lesser in the iris; ciliary body; and salivary, sweat, and bronchial glands.
The respiratory effects of atropine include reducing the volume of secretions from the nose, mouth, pharynx, and bronchi and relaxing smooth muscles of the bronchi and bronchioles, which decrease airway resistance. Since atropine is a potent bronchodilator, it is especially effective in blocking the acetylcholine-induced stimulation of guanyl cyclase, which is responsible for producing cyclic guanosine monophosphate (cGMP), a mediator of bronchoconstriction released from mast cells. These actions of atropine are useful, but controversial, in the treatment of antigen-, methacholine-, and exercise-induced bronchospasm in asthmatic patients.
PHARMACOKINETICS
Atropine is administered via oral, parenteral, endotracheal, oral inhalation, or ophthalmic routes.
After absorption, the drug is widely distributed throughout the body and crosses the blood-brain barrier and the placenta. It is metabolized in the liver to several metabolites including tropic acid. The initial half-life of atropine is about 2 to 3 hours, and the terminal half-life is about 12.5 hours. Atropine and metabolites are primarily excreted renally and, to a lesser extent, by the pulmonary and fecal routes.
Oral Route
Atropine is well absorbed after oral administration. Peak plasma concentrations are seen within 1 hour after oral administration.
Intramuscular Route
Atropine is well absorbed after intramuscular administration. Peak plasma concentrations are seen within 30 minutes following IM administration.
Inhalation Route
Atropine is well absorbed after oral inhalation. Following oral inhalation, peak plasma concentrations are reached in 1.5 to 4 hours.
Other Route(s)
Atropine is well absorbed after endotracheal administration
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