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Examination of the Potential Antiulcer Activity of the Calcium Antagonist Propyl-Methylenedioxyindene
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Since propyl-methylenedioxyindene (pr-MDI) exhibits significant protective effects against stress-induced ulcers in rats at subcardiovascular doses (10–30 mg/kg, i.p.), the aim of the present study was to explore the effect of this intracellular calcium antagonist on cysteamine-induced duodenal ulcers at the same low doses. Duodenal ulcers were induced in rats with a single dose of cysteamine (425 mg/kg, s.c), which produced an 80% ulcer incidence within 24 h without affecting gastric acid concentration. Administration of pr-MDI (10 and 30 mg/kg, i.p.) at 0, 6 and 12 h post-cysteamine did not afford protection against ulceration. On the other hand, atropine (10 mg/kg, s.c, administered at 0, 6 and 12 h post-cysteamine) resulted in a 69% inhibition of ulceration, and the antacid Maalox (2 ml, administered p.o. at 0, 2,4, 6 and 12 h post-cysteamine) completely prevented ulceration. The failure of pr-MDI to protect against duodenal ulceration is discussed in relation to its pharmacological mechanism of action and the pathogenetic mechanism of action of cysteamine.
Title: Examination of the Potential Antiulcer Activity of the Calcium Antagonist Propyl-Methylenedioxyindene
Description:
Since propyl-methylenedioxyindene (pr-MDI) exhibits significant protective effects against stress-induced ulcers in rats at subcardiovascular doses (10–30 mg/kg, i.
p.
), the aim of the present study was to explore the effect of this intracellular calcium antagonist on cysteamine-induced duodenal ulcers at the same low doses.
Duodenal ulcers were induced in rats with a single dose of cysteamine (425 mg/kg, s.
c), which produced an 80% ulcer incidence within 24 h without affecting gastric acid concentration.
Administration of pr-MDI (10 and 30 mg/kg, i.
p.
) at 0, 6 and 12 h post-cysteamine did not afford protection against ulceration.
On the other hand, atropine (10 mg/kg, s.
c, administered at 0, 6 and 12 h post-cysteamine) resulted in a 69% inhibition of ulceration, and the antacid Maalox (2 ml, administered p.
o.
at 0, 2,4, 6 and 12 h post-cysteamine) completely prevented ulceration.
The failure of pr-MDI to protect against duodenal ulceration is discussed in relation to its pharmacological mechanism of action and the pathogenetic mechanism of action of cysteamine.
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