Step 1: Understanding the Concept:
Anticholinergic agents (such as atropine and glycopyrrolate) act as competitive antagonists at muscarinic acetylcholine receptors throughout the body.
Their administration leads to parasympatholytic effects, including decreased secretions, bronchodilation, decreased gastrointestinal motility, and increased heart rate.
Step 2: Detailed Explanation:
When an anticholinergic like atropine is administered intravenously to dogs, a transient bradycardia (not tachycardia) often occurs initially.
This temporary slowing of the heart rate is caused by central vagal stimulation or presynaptic muscarinic (M1) receptor blockade, which increases acetylcholine release before peripheral muscarinic (M2) blockade on the sinoatrial node is fully established.
This initial phase can also manifest as temporary first-degree or second-degree atrioventricular (AV) blocks before progressing to the expected sustained sinus tachycardia.
In horses, anticholinergics significantly reduce gastrointestinal motility, which can lead to functional ileus and severe, potentially fatal colic.
At clinical doses, tertiary amines like atropine cross the blood-brain barrier and typically cause mild central nervous system stimulation rather than depression, though extremely high toxic doses may eventually lead to depression and coma.
Therefore, transient bradycardia is associated with initial administration, making transient tachycardia incorrect as a transient phenomenon.
Step 3: Final Answer:
The effect not associated with anticholinergic administration is transient tachycardia, as the transient phase is characterized by bradycardia.