Guth P H, Paulsen G, Nagata H
Gastroenterology. 1984 Nov;87(5):1083-90.
The effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) on histologic and microcirculatory changes in alcohol-induced gastric mucosal injury was studied. A histologic study confirmed that dmPGE2 does not protect the surface mucous cells against ethanol injury but does protect against the deeper necrotic lesion. Both the gross injury and the necrotic lesion were as severe after 1 min of ethanol exposure as after 60 min. A study of benzidine-stained sections and hematoxylin and eosin-stained sections revealed marked engorgement of microvessels and hemorrhage in the superficial mucosa after ethanol injury. Pretreatment with dmPGE2 prevented these. An in vivo fluorescent microscopy study revealed that there was total stasis of blood flow in the injured area. After the intravascular injection of a fluorescein-albumin conjugate, the conjugate filled microvessels in grossly normal areas of mucosa but not in grossly injured areas. Pretreatment with dmPGE2 prevented this microcirculatory change. This alcohol-induced stasis of flow in injured areas may be of pathogenetic significance and prostaglandin protection might involve prevention of this microcirculatory change.
研究了16,16 - 二甲基前列腺素E2(dmPGE2)对酒精诱导的胃黏膜损伤中组织学和微循环变化的影响。组织学研究证实,dmPGE2不能保护表面黏液细胞免受乙醇损伤,但能防止更深层的坏死病变。乙醇暴露1分钟后的大体损伤和坏死病变与60分钟后的一样严重。对联苯胺染色切片以及苏木精和伊红染色切片的研究显示,乙醇损伤后浅表黏膜微血管明显充血和出血。用dmPGE2预处理可防止这些情况。一项体内荧光显微镜研究显示,损伤区域血流完全停滞。血管内注射荧光素 - 白蛋白偶联物后,偶联物填充了黏膜大体正常区域的微血管,但未填充大体损伤区域的微血管。用dmPGE2预处理可防止这种微循环变化。这种酒精诱导的损伤区域血流停滞可能具有致病意义,前列腺素的保护作用可能涉及预防这种微循环变化。