Laudanno O M, Cesolari J A, Bedini O A, San Miguel P
Cátedras de Patología Médica III, Facultad de Ciencias Médicas, Rosario, Argentina.
Acta Gastroenterol Latinoam. 1990;20(2):89-92.
The unknown mechanism of adaptative gastric cytoprotection (AGC) induced by 20% ethanol and subsequent injury with 70% ethanol was studied in wistar rats. Pretreatment with indomethacin or HgII2 did not prevent the AGC, there suggesting that neither endogenous PGS nor gastric mucus take part in its mechanism. On the other hand, ranitidine pretreatment blocked and even aggravated the damage induced by ethanol-ethanol. In contrast, the latter phenomenon was reverted by 20% acidified ethanol. It is concluded that a back diffusion of H+ and bicarbonate play important roles in the AGC mechanism.
在Wistar大鼠中研究了20%乙醇诱导的适应性胃细胞保护（AGC）及其后70%乙醇损伤的未知机制。用吲哚美辛或HgII2预处理并不能预防AGC，这表明内源性前列腺素（PGS）和胃黏液均未参与其机制。另一方面，雷尼替丁预处理可阻断甚至加重乙醇诱导的损伤。相反，20%酸化乙醇可逆转后一种现象。得出结论，H+和碳酸氢根的反向扩散在AGC机制中起重要作用。
