How does morphine work on colonic motility? An electromyography study in human left and sigmoid colon
Centre Hospitalier Universitaire Sherbrooke, Québec, Canada J1H 5N4Life Sciences (Impact Factor: 2.7). 03/1986; 38(8):671-6. DOI: 10.1016/0024-3205(86)90580-1
The effect of morphine on colonic motility was investigated by recording the colonic myoelectric spiking activity by means of a 50 cm long silastic tube equipped with 4 bipolar AgAgCl ring electrodes fixed at 10 cm intervals that was introduced into the left colon in 8 healthy subjects by flexible sigmoidoscopy. Tracings were obtained for 1 hour in the fasting state and for another 1 hour after i.m. injection of morphine sulphate 0.15 mg/kg. The different types of spike bursts were compared before and after morphine injection. The control tracings showed that the spiking activity of the colon was made of 2 types: 1)- Rhythmic Stationary Spike Bursts (RSB), that were seen at only one electrode site; 2)- Sporadic Bursts, that were either propagating over all 4 electrodes (SPB) or non propagating (SNPB). Injection of morphine was followed by 1)- a considerable increase in the number of RSB from 107 +/- 43 bursts/hour (mean +/- SEM) to 491 +/- 23 bursts/hour; 2)- the complete disappearance of the SPB dropping from 7.3 +/- 2.0 bursts/hour to 0.3 +/- 0.2 bursts/hour; 3)- no significant change in SNPB (from 52 +/- 4 bursts/hour to 57 +/- 5 bursts/hour). These results indicate that 1)- stimulation of colonic smooth muscle activity by morphine seems to result from an increase in the number of rhythmic stationary bursts; 2)- however inhibition of colonic transit may be related to the decrease in the number of sporadic propagating bursts.
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ABSTRACT: The effects of vasopressin on colonic motility were investigated in 6 healthy subjects and 10 patients with chronic idiopathic constipation. Recordings of the colonic myoelectric spiking activity were performed by means of 50-cm long silastic tube, equipped with four bipolar ring electrodes fixed at 10-cm intervals, which was introduced by flexible colonoscopy into the left colon. Tracing were obtained for 1 h in the fasting state and for another hour after an intramuscular injection of a pharmacological dose of vasopressin (0.3 U/kg). The different types of spike bursts generated by the colonic smooth muscle were compared before and after vasopressin injection. In both controls and patients, the tracing showed (i) rhythmic stationary spike bursts (RSB) that were seen at only one electrode site; and (ii) sporadic bursts that were either propagating over all four electrodes (SPB) or nonpropagating (SNPB). Injection of vasopressin in controls was followed for 30 min by a significant increase in the number of propagating bursts from 2.7 +/- 0.6 (mean +/- SEM) to 5.2 +/- 1.4 bursts (p less than 0.05); RSB and SNPB were not altered by vasopressin. In the constipated patients, the number of propagating bursts during the control period was significantly lower (0.8 +/- 0.2 bursts/30 min) than in the volunteers (p less than 0.05). After vasopressin, there was a significant increase to 3.6 +/- 0.8 bursts/30 min (p less than 0.001); RSB and SNPB also did not show significant alteration after vasopressin. Finally, 4 out of the 10 patients passed stools during the recording session.(ABSTRACT TRUNCATED AT 250 WORDS)
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ABSTRACT: Opioid peptides and opioid receptors are distributed along the gastrointestinal (GI) tract, indicating endogenous opiates released peripherally may modulate GI motor and secretory functions. Animal studies have revealed that the effects of opiates on gut motility depend on the nature of the subclasses of receptor involved, the species and the part of bowel. Most opiates that have a selective or predominant mu agonist activity inhibit gastric motility and delay gastric emptying by acting centrally; delta and kappa agonist are inactive when injected systemically. The effect of opiates in delaying intestinal transit observed in man, rat and other species is related to an inhibition (rat) or a stimulation (dog and man) of intestinal contractions as premature phase III-like sequences. The constipating effects of morphine probably result mainly from its action on colonic motility. Morphine stimulates colonic motility in humans by action on both central and peripheral sites. This increase in colonic motility and the delay in colonic transit is associated with a reinforcement of tonic contractions and reduced propulsive waves. Opioid peptides have been shown to participate in the colonic motor response to eating in man and animals. Both delta and mu receptors are involved in the stimulatory effects of opiates on colonic motility, while kappa receptors inhibit colonic contractions, mainly by acting centrally. The effects of opiates on gastric acid secretion are still controversial but it has been well demonstrated that opiates act centrally to reduce pancreatic secretion in rats. Opiates also inhibit intestinal secretions via an action on the enteric nervous system as well as in the CNS. All these results reinforce the hypothesis that opioid peptides have a major physiological role in the control of gut motility and secretions, and these actions explain most of the pharmacological effects of opiate substances on the digestive tract.
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