Galli S J, Wershil B K, Bose R, Walker P A, Szabo S
Am J Pathol. 1987 Jul;128(1):131-40.
The authors used stereomicroscopy and planimetry to measure the area of glandular stomach mucosa acutely injured by oral ethanol in mast cell-deficient and congenic normal (+/+) mice, and examined the damaged areas in 1-mu sections. Ethanol caused degranulation and/or disruption of gastric mucosal mast cells, and, at certain concentrations of ethanol, mast cell-deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice developed significantly less (43-90% less) acute gastric injury than either congenic +/+ mice or WBB6F1-W/Wv mice whose mast cells were restored by bone marrow transplantation from WBB6F1-+/+ mice. Nevertheless, ethanol produced detectable, and in some cases substantial, gastric injury even in the complete absence of mast cells. Thus, ethanol can produce some damage to the gastric mucosa independently of mast cells. But these data suggest that under certain circumstances mast cells can augment the area of acute gastric injury induced by ethanol.
作者使用体视显微镜和面积测量法，对肥大细胞缺陷型和同基因正常（+/+）小鼠经口服乙醇急性损伤的腺胃黏膜面积进行测量，并在1微米切片中检查损伤区域。乙醇导致胃黏膜肥大细胞脱颗粒和/或破坏，在某些乙醇浓度下，肥大细胞缺陷型的WBB6F1-W/Wv或WCB6F1-Sl/Sld小鼠发生的急性胃损伤明显少于同基因+/+小鼠或通过从WBB6F1-+/+小鼠进行骨髓移植而恢复了肥大细胞的WBB6F1-W/Wv小鼠（减少43%-90%）。然而，即使在完全没有肥大细胞的情况下，乙醇也会造成可检测到的、在某些情况下是严重的胃损伤。因此，乙醇可独立于肥大细胞对胃黏膜造成一些损伤。但这些数据表明，在某些情况下，肥大细胞可增大乙醇诱导的急性胃损伤面积。
