Heart Although the dominant response to atropine is tachycardia, the heart rate often decreases slightly (4-8 beats/min) transiently with average clinical doses (0.4-0.6 mg). The slowing is usually absent after rapid intravenous injection. Larger doses of atropine cause progressively increasing tachycardia by blocking vagal effects on M2 receptors on the SA node. Resting heart rate increased by 35-40 beats/min in young men given 2 mg of atropine intramuscularly. The maximal heart rate (e.g., in response to exercise) is not altered by atropine. The influence of atropine is most noticeable in healthy young adults, in whom vagal tone is considerable. In infancy and old age, even large doses of atropine may fail to accelerate the heart. Atropine often produces cardiac arrhythmias, but without significant cardiovascular symptoms.
With low doses of scopolamine (0.1-0.2 mg), the cardiac slowing is greater than with atropine. With higher doses, a transient cardioacceleration may be observed.
Adequate doses of atropine can abolish many types of reflex vagal cardiac slowing or asystole— for example, from inhalation of irritant vapors, stimulation of the carotid sinus, pressure on the eyeballs, peritoneal stimulation, or injection of contrast dye during cardiac catheterization. Atropine also prevents or abruptly abolishes bradycardia or asystole caused by choline esters, acetylcholinesterase inhibitors, or other parasympathomimetic drugs, as well as cardiac arrest from electrical stimulation of the vagus. The removal of vagal influence on the heart by atropine also may facilitate AV conduction.
Circulation Atropine, alone, has little effect on blood pressure, an expected result since most vessels lack cholinergic innervation. However, in clinical doses, atropine completely counteracts the peripheral vasodilation and sharp fall in blood pressure caused by choline esters. Atropine in toxic, and occasionally therapeutic, doses can dilate cutaneous blood vessels, especially those in the blush area (atropine flush).
RESPIRATORY TRACT Belladonna alkaloids inhibit secretions of the nose, mouth, pharynx, and bronchi, and thus dry the mucous membranes of the respiratory tract. Reduction of mucous secretion and mucociliary clearance resulting in mucus plugs are undesirable side effects of atropine in patients with airway disease. Inhibition by atropine of bronchoconstriction caused by histamine, bradykinin, and the eicosanoids presumably reflects the participation of parasympathetic efferents in the bronchial reflexes elicited by these agents. The ability to block the indirect bron-choconstrictive effects of these mediators that are released during attacks of asthma forms the basis for the use of anticholinergic agents, along with b-adrenergic receptor agonists, in the treatment of asthma (see Chapter 27).
GASTROINTESTINAL TRACT Atropine can completely abolish the effects of ACh (and other parasympathomimetic drugs) on the motility and secretions of the GI tract, but can only incompletely inhibit the effects of vagal impulses. This difference is particularly striking in the effects of atropine on gut motility. Preganglionic vagal fibers that innervate the GI tract synapse not only with postganglionic cholinergic fibers, but also with a network of noncholinergic intramural neurons. These neurons of the enteric plexus release numerous neurotransmitters and neuromodu-lators (e.g., 5-HT, DA, myriad peptides) whose actions atropine does not block and which can effect changes in motility. Similarly, while vagal activity modulates gastrin-elicited histamine release and gastric acid secretion, the actions of gastrin can occur independently of vagal tone. Histamine H2 receptor antagonists and proton pump inhibitors have replaced nonselective muscarinic antagonists as inhibitors of acid secretion (see Chapter 36).
Salivary secretion, mediated through M3 receptors, is particularly sensitive to inhibition by muscarinic receptor antagonists, which can completely abolish the copious, watery, parasympathetically induced secretion. The mouth becomes dry, and swallowing and talking may become difficult. Gastric secretions during the cephalic and fasting phases are reduced markedly by muscarinic antagonists; the intestinal phase of gastric secretion is only partially inhibited. Atropine also reduces the cytoprotective secretions (HCO-, mucus) of the superficial epithelial cells (see Figure 36-1).
The parasympathetic nerves enhance both tone and motility and relax sphincters, thereby favoring intestinal transit. Muscarinic antagonists produce prolonged inhibitory effects on the motor activity of the GI tract; relatively large doses are needed to produce such inhibition. The complex myenteric nervous system can regulate motility independently of parasympathetic control, however (see Chapter 6).
Muscarinic antagonists decrease the normal tone and amplitude of contractions of the ureter and bladder, and often eliminate drug-induced enhancement of ureteral tone, but at doses of atropine that inhibit salivation and lacrimation and cause blurring of vision (Table 7-2). Control of bladder contraction is complex, involving mainly M2 receptors at multiple sites and also M3 receptors that can mediate detrusor muscle contraction.
Atropine exerts a mild antispasmodic action on the gallbladder and bile ducts, an effect that usually is insufficient to overcome or prevent the marked spasm and increase in biliary duct pressure induced by opioids, for which nitrites (see Chapter 31) are more effective.
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