Spenney J G, Bhown M
Gastroenterology. 1977 Oct;73(4 Pt 1):785-9.
The effects of acetylsalicylic acid on the in vitro bullfrog gastric mucosa were defined. After mucosal exposure of 10 or 20 mM acetylsalicylic acid, a characteristic series of changes evolved. The potential difference and resistance rose initially. After 15 to 30 min the potential difference declined to zero. Transmucosal resistance remained elevated considerably longer but began to decline toward zero after 30 to 60 min of exposure. Mucosal permeability to mannitol increased as transmucosal resistance declined, but was not markedly elevated until the 2nd hr of exposure to acetylsalicylic acid. The initial rise of potential difference was associated with inhibition of H+ secretion whereas the later decline of potential difference was due to inhibition of Cl- transport. The abolition of short circuit current could not be attributed to mucosal to serosal flux of acetylsalicylate.
确定了乙酰水杨酸对体外牛蛙胃黏膜的影响。在黏膜暴露于10或20 mM乙酰水杨酸后,出现了一系列特征性变化。电位差和电阻最初升高。15至30分钟后,电位差降至零。跨黏膜电阻在相当长的时间内仍保持升高,但在暴露30至60分钟后开始向零下降。随着跨黏膜电阻下降,黏膜对甘露醇的通透性增加,但直到暴露于乙酰水杨酸2小时后才明显升高。电位差的最初升高与H⁺分泌的抑制有关,而电位差随后的下降是由于Cl⁻转运的抑制。短路电流的消失不能归因于乙酰水杨酸从黏膜到浆膜的通量。