The anticholinergic drugs
While numerous anticholinergic drugs exist, in anesthesia we deal almost exclu-sively with atropine and glycopyrrolate, and occasionally with scopolamine. All three drugs act on the autonomic nervous system, blocking the effect of acetyl-choline at post-ganglionic nerve endings. Thus, they accelerate heart rate (if sym-pathetic tone is present and capable of accelerating heart rate), bronchodilate, cause mydriasis (thereby increasing intraocular pressure), inhibit salivation (and in the process dry secretions in the upper airway), inhibit sweating (by block-ing the effect of postganglionic sympathetic cholinergic stimulation), and exert a variety of effects on the GI and GU systems. In anesthesia we use atropine or glycopyrrolate to counteract bradycardia, salivation, and intestinal cramping, all of which are side effects of neostigmine.
Atropine and scopolamine are tertiary amines and thus capable of crossing the blood–brain barrier. In the elderly, scopolamine often causes delirium. Both drugs cross the placenta, and atropine has been observed to accelerate fetal heart rate. Both drugs have a dual effect – in addition to their well-recognized peripheral anti-cholinergic effect, they have a stimulating central vagal effect. With scopolamine, we sometimes see bradycardia when the central stimulating effect outlasts the peripheral blocking effect of the drug. Glycopyrrolate is a quaternary, charged compound and thus largely prevented from crossing the blood–brain barrier or the placenta.