Puurunen J, Huttunen P, Hirvonen J
Acta Pharmacol Toxicol (Copenh). 1983 May;52(5):321-7. doi: 10.1111/j.1600-0773.1983.tb01110.x.
The interactions between ethanol (EtOH) and acetylsalicylic acid (ASA) in damaging the gastric mucosa were investigated in urethane-anaesthetised rats upon intragastric irrigation. The addition of 5, 10 or 20 mM ASA to 1 and 4 M EtOH instillates strongly aggravated lesion formation in the gastric mucosa and mucosal bleeding. ASA enhanced the back-diffusion of hydrogen ions into the mucosa induced by 1 M EtOH, whereas gastric mucosal blood flow, which is thought to dispose of the back-diffused acid from the mucosa, remained unchanged, thus resulting in an accumulation of acid within the gastric mucosa. ASA did not further enhance the strongly increased back-diffusion of hydrogen ions induced by 4 M EtOH, but it effectively inhibited EtOH-induced stimulation of the gastric mucosal blood flow, thus causing an increase in the ratio between hydrogen ion back-diffusion and gastric mucosal blood flow. The simultaneous presence of EtOH and ASA did not enhance the rates of absorption of each from the instillates. The results indicate that EtOH and ASA have a strong synergistic action in damaging the gastric mucosa in the rat. The mechanism of this interaction may be an increased accumulation of hydrogen ions within the gastric mucosa, resulting in excessive acidification of the mucosal tissue.
在经氨基甲酸乙酯麻醉的大鼠中，通过胃内灌注研究了乙醇（EtOH）和乙酰水杨酸（ASA）对胃黏膜损伤的相互作用。在1 M和4 M乙醇灌洗液中添加5、10或20 mM ASA会强烈加重胃黏膜损伤的形成和黏膜出血。ASA增强了1 M乙醇诱导的氢离子向黏膜的反向扩散，而被认为可处理从黏膜反向扩散的酸的胃黏膜血流量保持不变，从而导致胃黏膜内酸的积累。ASA并未进一步增强4 M乙醇诱导的氢离子强烈增加的反向扩散，但它有效地抑制了乙醇诱导的胃黏膜血流量的刺激，从而导致氢离子反向扩散与胃黏膜血流量的比率增加。乙醇和ASA同时存在并未提高它们从灌洗液中的吸收速率。结果表明，乙醇和ASA在损伤大鼠胃黏膜方面具有强烈的协同作用。这种相互作用的机制可能是胃黏膜内氢离子积累增加，导致黏膜组织过度酸化。
