Glycopyrronium bromide

• Glycopyrronium
• Glycopyrrolate

IUPAC: 3 - (2 -cyclopentyl -2-hydroxy -2- phenylacetoxy ) -1,1 - dimethylpyrrolidiniumbromid

A03AB02

Anticholinergic

From 193.2 to 194.5 ° C

709 mg · kg -1 ( LD50, rat, oral)

Template: Infobox chemical / molecular formula search available

Glycopyrrolate ( Robinul ® trade name, for inhalation Seebri ®) belongs to the group of parasympatholytics. Without glycopyrronium counterion is also known as glycopyrrolate.

• 2.1 Mechanism of action ( pharmacodynamics )
• 2.2 Absorption and distribution in the body ( pharmacokinetics )

Clinical information

Areas of application (indications )

• Secretion impairment (eg, drooling, pseudo - hypersalivation, terminal rattle breathing).
• Colic, inoperable bowel obstruction.
• Before surgery to reduce the flow of saliva, the secretion of the pharynx, in the trachea and in the bronchial
• Reducing the amount of gastric juice and free acid.
• Blockade of the delayed reflex of the vagus on the heart during anesthesia induction and intubation.
• To protect against side effects of cholinergics ( Bronchorrhoe, bronchospasm, bradycardia and excessive bowel activity ), which are given for reversal of neuromuscular blockade of non-depolarising muscle relaxants.
• Inhalation for the treatment of chronic obstructive pulmonary disease.

Adverse effects (side effects)

The peripheral anticholinergic effects include, in particular constipation, decreased sweating, dryness of mouth, nose and throat. At the application site irritation or inflammation can occur.

Pharmacological properties

Mechanism of action ( pharmacodynamics )

Glycopyrronium bromide competitively inhibits the effects of acetylcholine at muscarinic cholinergic neurons ( postganglionic ). It is a competitive antagonism at muscarinic receptors (M- Cholinorezeptoren ). These peripheral cholinergic receptors are located in the autonomous effector cells of the smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands and in limited extent, in the autonomic ganglia. In the pharynx, in the trachea and in the bronchi, excessive secretion production is limited. The muscarinic receptors in the salivary glands weigh heavily on anticholinergics. Inhibition of salivary secretion occurs already at a dose one, do not occur in the other unwanted anticholinergic effects, that is, the probability of the occurrence of side effects for this indication is less. A reduction of the increased salivary flow often results in an improvement in the ability to speak.

Uptake and distribution in the body ( pharmacokinetics )

Glycopyrronium is a synthetic, ionized (low lipid solubility ), quaternary ammonium anticholinergic, which happened cell membranes poorly. According hard penetrated glycopyrronium in the CNS or in the ocular tissue. Side effects such as sedation or delirium can be found by rare ( blood -brain barrier ). The oral absorption is poor, the potency ratio of i -v.- injection to oral is about 35:1. Nevertheless, lead 200-400 micrograms Glycopyrronium p. o tds to plasma concentrations that inhibit salivary up to 7 hours. Intravenously, glycopyrronium for inhibition of secretion is two to five times more potent than scopolamine hydrobromide. Therefore, it may also in some patients who do not respond to scopolamine, leading to inhibition of secretion. However, the effectiveness of scopolamine hydrobromide, hyoscine butylbromide and glycopyrronium as antisecretory agent is generally comparable. A terminal rattle breathing is improved when one-third to half of the patients. The optimal parenteral single dose is 200 micrograms. Compared to the onset of action of scopolamine hydrobromide Glycopyrronium slower. It has due to its lower affinity for muscarinic type 2 fewer cardiac side effects. Although in standard doses, although intraocular pressure or pupil size are not changed by Glycopyrronium, it may favor a narrow-angle glaucoma. The elimination is via the kidneys. Thus, lower dosages are already effective in patients with renal failure.