These drugs inhibit the degradation of ACh by its esterase (see Chapter 8), thereby allowing ACh to accumulate at sites of release. Unlike muscarinic receptor agonists, these parasympath-omimetic drugs do not stimulate muscle directly, but rather accelerate GI transit times by enhancing the contractile effects of ACh released at synaptic and neuromuscular junctions. Among these cholinergic muscle stimulants, neostigmine methylsulfate has been used off-label for some GI disorders, particularly those associated with acute colonic pseudo-obstruction (Ogilvie's syndrome) and paralytic ileus. The usual dose in the acute setting is 2—2.5 mg of neostigmine administered intravenously over 3 minutes with continuous monitoring of ECG, blood pressure, and O2 saturation. Atropine should be available in case of severe bradycardia.
Dopamine is present in significant amounts in the GI tract and has several inhibitory effects on motility, including reduction of lower esophageal sphincter and intragastric pressures. These effects, which apparently result from suppression of ACh release from myenteric motor neurons, are mediated by D2 receptors. By antagonizing the inhibitory effect of dopamine on myenteric motor neurons,
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...