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Pepsin release by prostaglandin E1 analogue. A potential therapeutic problem
M D Basson1, K A Zucker, T E Adrian
1Department of Surgery, Yale University School of Medicine, New Haven, Conn.
Archives of Surgery (Chicago, Ill. : 1960)
|April 1, 1988
Summary
Prostaglandin E1 analogue misoprostol inhibits gastric acid secretion but stimulates pepsinogen release in rabbit gastric glands. This dual action may impact the effectiveness of prostaglandins in healing peptic ulcers.
Area of Science:
- Gastroenterology
- Pharmacology
Background:
- Prostaglandins inhibit gastric acid secretion and offer cytoprotection for the gastric mucosa.
- They are being investigated for peptic ulcer treatment.
Purpose of the Study:
- To investigate the effects of misoprostol, a prostaglandin E1 analogue, on pepsinogen and acid secretion in isolated rabbit gastric glands and parietal cells.
Main Methods:
- Pepsinogen secretion was measured using iodine 125-labeled albumin digestion.
- Acid secretion was assessed indirectly via carbon 14-tagged aminopyrine uptake.
- Experiments were conducted on isolated rabbit gastric glands and enriched parietal cells.
Main Results:
- Misoprostol inhibited histamine-stimulated acid secretion in parietal cells (50% inhibition at 10(-9) mol/L, 78% at 10(-7) mol/L).
- Conversely, misoprostol significantly stimulated pepsinogen secretion in gastric glands (half-maximal effect at 10(-8) mol/L, 227% maximal stimulation at 10(-6) mol/L).
Conclusions:
- Misoprostol exhibits a dual effect: inhibiting acid secretion while stimulating pepsinogen release.
- The stimulated pepsin release could potentially compromise the ulcer-healing efficacy of prostaglandins.