Antiulcer effect of diltiazem in rats.
OBJECTIVE
To study the effects of diltiazem (Dil) on several experimental gastric ulcers in rats.


METHODS
The gastric mucosa damage was induced by indometacin (Ind), restraint, pyloric ligation, and absolute ethanol in rats. Dil 5, 25, 50 mg . kg-1 ig bid for 5 times. The number of gastric ulcers, the secretion of gastric juice, hydrochloric acid (HCI), and pepsin A were detected. The production of malondialdehyde (Mal) and the activity of superoxide dismutase (SOD) in gastric mucose were examined.


RESULTS
Dil 5, 25, 50 mg . kg-1 ig protected the gastric mucosa against the damages in a dose-dependent manner. Dil inhibited the secretion of gastric juice, HCI, pepsin A, and Mal production of the gastric mucosa, but increased the activity of SOD in the gastric mucosa. The production of Mal was decreased from 9.3 +/- 3.7 to 6.5 +/- 1.9 mumol/g wet weight (P < 0.05) and the activity of SOD was increased from 6.1 +/- 5.6 to 12.8 +/- 2.8 kU/g protein (P < 0.01) by Dil 50 mg . kg-1.


CONCLUSIONS
The inhibition of gastric secretion and lipid peroxidation induced by oxygen free radicals of gastric mucosa was related to the antiulcer effect of Dil in rats.
Yong
D G
DG
Department of Pharmacology, Zhejiang Medical University, Hangzhou, China.
Geng
B Q
BQ
Li
Y
Y
Bi
S
S
D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology*; D004110:Diltiazem / Q000494:pharmacology*; D005260:Female; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010434:Pepsin A / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism
D000897:Anti-Ulcer Agents; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D010434:Pepsin A; D004110:Diltiazem