Bou-Abboud C F, Wayland H, Paulsen G, Guth P H
Medical Service, VA Medical Center, West Los Angeles, California.
Dig Dis Sci. 1988 Jul;33(7):872-7. doi: 10.1007/BF01550978.
The relation of blood flow stasis to the development of unequivocal histologic necrosis (loss of parietal cells from the column of contiguous cells) in ethanol-induced gastric mucosal injury was studied in anesthetized rats. The most rapid vascular change that occurred when the gastric mucosa was exposed to 100% ethanol was a severe segmental constriction of the large submucosal venules. At 22 sec, the average venular diameter was 52.2 +/- 6.0% of the original one. This was followed by complete superficial mucosal blood flow stasis at 49 +/- 4 sec and appearance of histologic evidence of necrosis in one of seven rats at 2.5 min, four of six rats at 10 min, and seven of seven rats at 60 min. We conclude that in ethanol-induced gastric mucosal injury, submucosal venular constriction occurs first, followed by cessation of mucosal blood flow to be followed later on with histologic evidence of necrosis.
在麻醉大鼠中研究了血流淤滞与乙醇诱导的胃黏膜损伤中明确的组织学坏死（连续细胞柱中壁细胞丢失）发生之间的关系。当胃黏膜暴露于100%乙醇时，发生的最迅速的血管变化是大的黏膜下小静脉严重节段性收缩。在22秒时，小静脉平均直径为原来的52.2±6.0%。随后在49±4秒时出现完全的浅表黏膜血流淤滞，在2.5分钟时7只大鼠中有1只出现组织学坏死证据，10分钟时6只大鼠中有4只出现，60分钟时7只大鼠全部出现。我们得出结论，在乙醇诱导的胃黏膜损伤中，首先发生黏膜下小静脉收缩，随后黏膜血流停止，之后出现组织学坏死证据。
