Cho C H, Ogle C W
Eur J Pharmacol. 1978 Mar 1;48(1):97-105. doi: 10.1016/0014-2999(78)90047-x.
The effects on zinc sulphate pretreatment of rats on stress-induced gastric ulcers and on changes in mast cell counts were studied and correlated with changes in gastric mucosal microcirculation. The effects on zinc sulphate on blood pressure responses and on growth were also examined. Stress (2 h restraint at 4 degrees C) produced marked glandular mucosal ulceration, lowered the stomach wall mast cell counts and increased the microcirculatory blood volume in the superficial glandular mucosa. Zinc sulphate (22, 44 or 88 mg/kg; injected i.p. 48 h before stress) reversed all these changes in a dose-related manner. Blood pressure responses to i.v. acetylcholine, adrenaline or histamine were unaffected and growth of the rats as observed for 7 days after injection was not impaired. On the basis of these findings the mechanism of the antiulcer action of zinc sulphate is the following: inhibition of the stress-induced release of vasoactive agents from gastric mast cells and thus prevention of the subsequent microciculatory changes known to produce mucosal ulceration. Interference with vascular responses through direct blockade or toxicity is unlikely.
研究了硫酸锌预处理大鼠对应激性胃溃疡的影响以及肥大细胞计数的变化,并将其与胃黏膜微循环的变化相关联。还研究了硫酸锌对血压反应和生长的影响。应激(4℃下约束2小时)导致明显的腺性黏膜溃疡,降低胃壁肥大细胞计数,并增加浅表腺性黏膜的微循环血容量。硫酸锌(22、44或88mg/kg;在应激前48小时腹腔注射)以剂量相关的方式逆转了所有这些变化。静脉注射乙酰胆碱、肾上腺素或组胺后的血压反应未受影响,注射后7天观察到的大鼠生长也未受损。基于这些发现,硫酸锌抗溃疡作用的机制如下:抑制应激诱导的胃肥大细胞释放血管活性物质,从而预防随后已知会导致黏膜溃疡的微循环变化。通过直接阻断或毒性干扰血管反应的可能性不大。