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Morphine and gastroduodenal motility.
1Division of Gastroenterology, Jerry L. Pettis Memorial Veterans Medical Center, Loma Linda, California 92354, USA.
Digestive Diseases and Sciences
|November 26, 1999
Summary
Intravenous morphine stimulates duodenal motility, inducing phase III-like contractions. This effect is mediated by opioid receptors and blocked by antimuscarinic drugs, highlighting morphine
Area of Science:
- Gastroenterology
- Pharmacology
- Neurogastroenterology
Background:
- Opioid analgesics like morphine can affect gastrointestinal function.
- Understanding morphine's impact on duodenal motility is crucial for clinical practice.
Purpose of the Study:
- To investigate the effects of intravenous morphine on gastric antral and duodenal motility.
- To characterize the nature of morphine-induced duodenal contractions and their underlying mechanisms.
Main Methods:
- Healthy volunteers received intravenous morphine via infusion or bolus injection.
- Duodenal motility was monitored, and the effects of naloxone and atropine were assessed.
- Morphine's action was studied following spontaneous phase III activity and after a liquid meal.
Main Results:
- Intravenous morphine significantly increased duodenal motility, inducing phase III-like contractions.
- Naloxone, an opioid receptor antagonist, blocked morphine's effect.
- Atropine, an antimuscarinic agent, prevented morphine-induced duodenal activity.
Conclusions:
- Low-dose intravenous morphine potently stimulates duodenal contractility in a phase III-like manner.
- Morphine initiates this response via opioid receptors.
- The effect is mediated through a pathway sensitive to antimuscarinic drugs.