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  6. Endogenous Opioids Accumulate In Plasma In A Rat Model Of Acute Cholestasis.

Endogenous opioids accumulate in plasma in a rat model of acute cholestasis.

M G Swain1, R B Rothman, H Xu

  • 1Liver Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.

Gastroenterology
|August 1, 1992

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Summary
This summary is machine-generated.

Cholestasis significantly elevates plasma opioid activity and methionine-enkephalin levels in rats, suggesting endogenous opioids play a role in the condition. Protection from degradation may contribute to these increased opioid levels.

Area of Science:

  • Biochemistry
  • Physiology
  • Pharmacology

Background:

  • Cholestasis, a condition of impaired bile flow, is associated with altered endogenous opioid system activity.
  • Understanding these changes is crucial for elucidating cholestasis pathophysiology.

Purpose of the Study:

  • To quantify changes in endogenous opioid activity in rats with acute cholestasis.
  • To investigate the specific role of methionine-enkephalin in elevated opioid levels during cholestasis.

Main Methods:

  • Acute cholestasis was induced in rats via bile duct resection.
  • Total plasma opioid activity was measured using a radioreceptor assay with [3H]-DAMGO.
  • Plasma methionine-enkephalin levels were quantified using radioimmunoassay and validated with HPLC.

Main Results:

  • Bile duct-resected rats showed a threefold increase in total plasma opioid activity compared to controls.
  • Plasma methionine-enkephalin levels were significantly elevated (6-fold vs. sham, 17-fold vs. unoperated).
  • Methionine-enkephalin constituted less than 5% of total opioid activity, and was stable in vitro, suggesting reduced degradation.

Conclusions:

  • Elevated plasma opioid activity and methionine-enkephalin levels are characteristic of cholestasis in rats.
  • Reduced degradation of methionine-enkephalin may contribute to its increased plasma concentration.
  • These findings support the hypothesis that endogenous opioids are involved in the pathophysiology of cholestasis.

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