Tarnawski A, Hollander D, Gergely H
VA Medical Center, Long Beach, California 90822.
Scand J Gastroenterol Suppl. 1990;174:9-14. doi: 10.3109/00365529009091925.
There is increasing evidence that aluminum-containing antacids are able to protect the gastric mucosa against various ulcerogenic and necrotizing agents including 0.6 M HCl, 0.2 M NaOH, and absolute alcohol. Since gastric mucosal necrosis produced by alcohol is independent of luminal acid and cannot be reduced by H2-receptor antagonists, the protective action of antacids is accomplished by mechanism(s) other than acid-neutralizing ability. In addition, since acidified antacids can protect the gastric mucosa even better than an antacid with intact neutralizing capacity, it is clear that such action is independent of acid-neutralizing ability and therefore has all the features of cytoprotection. Whereas the cytoprotective action of antacids in experimental conditions is well established, the mechanisms of antacid-induced mucosal protection are not known. The clinical relevance of antacid-induced protection also requires further elucidation. Antacids have advantages over the H2 blockers in protecting the gastric mucosa against alcohol-induced necrosis and in preventing stress-induced ulcers in critically ill patients. Although more work is needed to clarify the mechanisms of cytoprotective action of antacids, the recent experimental findings gave a new life to and new potential clinical applications for antacids.
越来越多的证据表明，含铝抗酸剂能够保护胃黏膜免受多种致溃疡和坏死物质的侵害，这些物质包括0.6 M盐酸、0.2 M氢氧化钠和无水乙醇。由于酒精引起的胃黏膜坏死与管腔内的酸无关，且不能被H2受体拮抗剂减轻，抗酸剂的保护作用是通过除中和酸能力之外的其他机制实现的。此外，由于酸化的抗酸剂比具有完整中和能力的抗酸剂能更好地保护胃黏膜，显然这种作用与中和酸的能力无关，因此具有细胞保护的所有特征。尽管抗酸剂在实验条件下的细胞保护作用已得到充分证实，但其诱导黏膜保护的机制尚不清楚。抗酸剂诱导保护的临床相关性也需要进一步阐明。在保护胃黏膜免受酒精诱导的坏死以及预防重症患者的应激性溃疡方面，抗酸剂比H2阻滞剂更具优势。尽管需要更多的研究来阐明抗酸剂细胞保护作用的机制，但最近的实验结果为抗酸剂带来了新的生机和新的潜在临床应用。
