ABSTRACT
The pharmacologic effects of opioids in the gastrointestinal (GI) tract include inhibition of gastric and intestinal motility, impaired defecation, and increased fluid absorption from the bowel.1 These symptoms have been attributed to several mechanisms involving both peripheral and central opioid receptors. Opioid receptors have been localized throughout the GI tract,2,3 and stimulation of these receptors by exogenous opioids has been shown to directly affect bowel function.4,5 Of the three most prominent opioid receptor subtypesmu, kappa, and delta-the mu opioid receptor is the primary target for pain management among most currently marketed opioid analgesics;6 these opioids maintain selectivity for the mu opioid receptor at
normal therapeutic doses.6 However, the mu opioid receptor also appears to be the primary mediator of decreased GI motility, thus causing a potential clinical trade-off between effective analgesia and management of adverse side effects.6
