A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Robinul Pharmacology, Pharmacokinetics, Studies, Metabolism - Glycopyrrolate
Robinul Pharmacology, Pharmacokinetics, Studies, Metabolism - Glycopyrrolate
CLINICAL PHARMACOLOGY
Glycopyrrolate, like other anticholinergic
(anti-muscarinic) agents, inhibits the action
of acetylcholine
on structures innervated by postganglionic cholinergic nerves and
on smooth muscles that respond to acetylcholine but lack cholinergic
innervation. These peripheral
cholinergic receptors
are present in the autonomic
effector cells of smooth
muscle, cardiac muscle,
the sinoatrial node,
the atrioventricular
node, exocrine glands,
and, to a limited degree, in the autonomic
ganglia. Thus, it diminishes the volume and free acidity of gastric
secretions and controls excessive pharyngeal, tracheal, and bronchial
secretions.
Glycopyrrolate antagonizes muscarinic
symptoms (e.g., bronchorrhea, bronchospasm, bradycardia, and intestinal
hypermotility) induced
by cholinergic drugs such as the anticholinesterases.
The highly polar quaternary
ammonium group
of glycopyrrolate
limits its passage across
lipid membranes, such as the blood- brain
barrier, in contrast to atropine sulfate
and scopolamine hydrobromide, which are non-polar tertiary amines
which penetrate lipid
barriers easily.
Peak effects occur approximately 30 to 45 minutes after intramuscular
administration. The vagal
blocking effects persist
for 2 to 3 hours and the antisialagogue
effects persist up to 7 hours, periods longer than for atropine.
With intravenous
injection, the onset of action
is generally evident within one minute.
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