Koo M W, Cho C H, Ogle C W
Eur J Pharmacol. 1986 Jan 29;120(3):355-8. doi: 10.1016/0014-2999(86)90477-2.
The effect of verapamil on ethanol-induced gastric ulceration was investigated in rats. Orally administered ethanol (0.5 ml), 10, 20 or 40% v/v, dose dependently produced glandular lesions, ranging from petechiae to haemorrhagic ulcers. These lesions were worsened by verapamil (2, 4 or 8 mg/kg given intraperitoneally (i.p.) 30 min beforehand) in the 30 min and 2 h ethanol-exposure experiments. However, ethanol ulceration or its aggravation by verapamil was antagonised by calcium gluconate (112 or 224 mg/kg given per os (p.o.) 30 min before ethanol administration) in a dose-related manner. These findings suggest that intracellular calcium depletion in the gastric glandular mucosa may account for ethanol ulceration and the ulcer-aggravating action of verapamil.
研究了维拉帕米对乙醇诱导的大鼠胃溃疡的影响。口服给予体积分数为10%、20%或40%的乙醇(0.5 ml),剂量依赖性地产生腺性病变,从瘀点到出血性溃疡不等。在30分钟和2小时乙醇暴露实验中,维拉帕米(预先30分钟腹腔注射(i.p.)2、4或8 mg/kg)使这些病变恶化。然而,葡萄糖酸钙(乙醇给药前30分钟口服(p.o.)112或224 mg/kg)以剂量相关的方式拮抗乙醇溃疡或维拉帕米对其的加重作用。这些发现表明,胃腺黏膜细胞内钙耗竭可能是乙醇溃疡和维拉帕米溃疡加重作用的原因。