The Effect of Acute and Chronic Administration of Morphine and Morphine Withdrawal on Intestinal Transit Time in the Rat

Brown, Nicola J.; Coupar, Ian M.; Rumsey, R. D. E.

doi:10.1111/j.2042-7158.1988.tb06286.x

Cited by 29 publications

(12 citation statements)

References 19 publications

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“…There is some evidence that morphine stimulates mucosal sensory receptors, which, in turn, activate a reflex arc to increase fluid absorption further [24]. The mechanism of the antisecretory effect of opioids has been shown to be indirect.…”

Section: Opioid Effects On the Gastrointestinal Tractmentioning

confidence: 99%

Constipation in advanced cancer patients

Mancini

Bruera

1998

Support Care Cancer

148

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Constipation is a frequent, distressing, and underestimated complication in patients with advanced cancer. It may develop from general disturbances that may or may not be cancer related, but the use of opioids is one of the main causes in this population. Opioids affect the intestine by reducing motility and secretions and by increasing fluid absorption and blood flow. Untreated constipation may lead to several complications. Effective management of constipation starts with a careful assessment of the patient, including the history of the frequency and difficulty of defaecation, symptoms caused by constipation, and physical and rectal examinations. When the diagnosis of constipation is unclear, an abdominal X-ray may be required. The treatment of constipation includes general interventions, such as the availability of comfort and privacy or the elimination of medical factors that may contribute to constipation, and therapeutic interventions including oral or rectal laxatives and the use of prokinetic drugs and naloxone. The purpose of this paper is to review the pathophysiology and causes of constipation and the effects of opioids on the gastrointestinal tract, and to propose an approach for its assessment and management. Randomized clinical trials between different laxatives and/or prokinetic agents in cancer patients are needed, and future studies should focus on the validation of different clinical assessment tools for constipation.

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Section: Opioid Effects On the Gastrointestinal Tractmentioning

confidence: 99%

Constipation in advanced cancer patients

Mancini

Bruera

1998

Support Care Cancer

148

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“…The diarrhoea that is produced on opiate withBrkish Joumal of Phannacology (1995) U4. 152-156 drawal in this species is associated with a decrease in intestinal fluid absortion (Chang et al, 1984) and increased intestinal motility (Brown et al, 1988 (Coupar & Hancock, 1994). The specific aim of this study was to characterize the receptor mediating one of these effects, namely inhibition of intestinal fluid secretion, using a range of metabolically stable adenosine analogues with different potencies and degrees of specifity for adenosine receptor subtypes.…”

Section: Introductionmentioning

confidence: 99%

Functional characterization of the adenosine receptor mediating inhibition of intestinal secretion

Hancock¹,

Coupar²

1995

British J Pharmacology

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Previous studies have shown that the mixed A1/A2 adenosine agonist 5′‐N‐ethylcarboxamido‐adenosine (NECA) inhibits intestinal fluid secretion which is thought to contribute to its antidiarrhoeal effect in the rat. The aim of this study was to characterize the adenosine receptor mediating this antisecretory effect via functional studies using a range of selective agonists and antagonists and by applying the pharmacological criteria of relative agonist and antagonist potencies. Adenosine agonists and antagonists were administered i.v. to anaesthetized rats. Intestinal secretion was then stimulated by i.a. infusion of vasoactive intestinal peptide (VIP, 0.8 μg min−1) and the net fluid transport across the wall of the jejunum was measured by a recirculation technique. The rank order of agonist potency to reduce the response to VIP was: NECA > N6‐cyclopentyladenosine (CPA) > R‐N6‐(2‐phenylisopropyladenosine) (R‐PIA) > S‐PIA > chloroadenosine (2‐CADO) > 2‐phenylaminoadenosine (CV‐1808). This order best complies with the rank order of agonist potency that represents activation of the recently described A2B receptor: NECA > 2‐CADO R‐PIA = CHA > S‐PIA > = CV‐1808 > = CGS‐21680. The most potent agonists (NECA, CPA and R‐PIA) had ED50 values in the low microgram range. The anitsecretory action of NECA (submaximal dose of 40μg kg−1) was antagonized equally (approximately 50%) by the selective adenosine antagonists 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX, 0.1 mg kg−1) and 8‐phenyltheophylline (8‐PT, 0.1 mg kg−1). This equipotent activity indicates the presence of an A2 and not an A1 receptor. It is suggested that adenosine A2B receptor agonists could be evaluated for potential use as antidiarrhoeal drugs.

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“…Naloxone was given to the animals subcuta neously in a volume of 0.25 ml of saline 30 min prior to commencing the experiment. The dose of naloxone chosen for this study w'as within the range used for this class of receptors and has previously been shown to antagonise either the effect of an opiate agonist or gas trointestinal motility [6,7], Experimental Protocol Breath Hydrogen Technique. A total of 8 animals were used for this part of the study.…”

Section: Preparation O F Test Substancesmentioning

confidence: 99%

The Effect of an Opiate Receptor Antagonist on the Heal Brake Mechanism in the Rat

et al. 1993

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Studies investigated the effect of the opiate antagonist naloxone (10 mg/kg) on stomach to caecum transit (SCTT) during ileal infusion of saline or Intralipid. SCTT of the head of the meal was measured by hydrogen analysis and meal distribution by the radiolabelled meal technique. Intralipid delayed SCTT by delaying both gastric emptying (p < 0.01) and small bowel transit. Naloxone did not affect SCTT during ileal saline infusion, but produced a distal shift (p < 0.05) in the geometric centre of the meal and increased radioactivity in the caecum (p < 0.001) 100 min after gavage. Naloxone abolished the delayed SCTT of the meal induced by ileal lipid infusion, with an associated increase in radioactivity in the caecum at 200 min (p < 0.01), although the geometric centre was shifted proximally within the intestine (p < 0.01). The results suggest that the ileal brake is mediated in part by endogenous opiate pathways.

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The Effect of Acute and Chronic Administration of Morphine and Morphine Withdrawal on Intestinal Transit Time in the Rat

Cited by 29 publications

References 19 publications

Constipation in advanced cancer patients

Constipation in advanced cancer patients

Functional characterization of the adenosine receptor mediating inhibition of intestinal secretion

The Effect of an Opiate Receptor Antagonist on the Heal Brake Mechanism in the Rat

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