Gastric Surface Epithelial Cell Damage Induced by Restraint and Water‐Immersion Stress in Rats: Protective Effects of 16, 16‐Dimethyl‐Prostaglandin E2
Gastric Surface Epithelial Cell Damage Induced by Restraint and Water‐Immersion Stress in Rats: Protective Effects of 16, 16‐Dimethyl‐Prostaglandin E2
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束缚和水浸应激引起的大鼠胃表面上皮细胞损伤：16, 16-二甲基-前列腺素 E2 的保护作用
DOI：
10.1097/00004836-198812001-00009
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发表时间：
1988
影响因子：
2.9
通讯作者：
S. Okabe
中科院分区：
文献类型：
--
作者：
T. Ohno;S. Okabe
研究了大鼠在束缚和水浸应激（22°C）下胃粘膜表面上皮细胞损伤和肉眼可见病变的时间过程，并将16，16-二甲基前列腺素E2（dmPGE 2）对胃粘膜表面上皮细胞损伤和肉眼可见病变的预防作用与罂粟碱、替莫拉唑和阿托品进行了比较。应激在可见损伤之前产生表面上皮细胞损伤，前者的严重程度随着时间的推移而增加，60 min后达到平台期，此时可观察到表面上皮细胞沿粘膜褶皱沿着脱落。与此相反，肉眼可见的病变出现2小时后的压力，严重程度继续增加，随着时间的推移。处理前注射（s.c.）dm-PGE 2（3和30 μg/kg）、罂粟碱（100 mg/kg）和阿托品（1 mg/kg）保护表面细胞免受应激诱导的损伤（1 h），并抑制应激4 h后可见的损伤形成。依普拉唑（30 mg/kg s.c.）不保护表面细胞，但明显抑制可见损伤形成。DMPGE 2，罂粟碱，阿托品，但不是替莫拉唑，抑制应激诱导的胃收缩增加。DMPGE 2，替莫拉唑，阿托品，但不罂粟碱，抑制酸分泌在应激条件下。这些结果表明，由于胃收缩增加，应激在1小时内诱导胃粘膜损伤，并且在酸存在下，表面上皮细胞损伤发展成肉眼可见的损伤，并且dmPGE 2可能通过抑制胃收缩来保护表面上皮免受应激诱导的损伤。
The time course of gastric mucosal surface epithelial cell damage and macroscopically visible lesions in response to restraint and water-immersion stress (22°C) in rats was examined, and the prophylactic effects on it of 16, 16-dimethyl-prostaglandin E2 (dmPGE2) were compared with those of papaverine, timoprazole, and atropine. The stress produced surface epithelial cell damage prior to visible lesion, the former increasing in severity with time and reaching a plateau 60 min later, by which time exfoliation of surface epithelial cells was observable along the mucosal folds. In contrast, macroscopically visible lesions appeared 2 h after stress, and severity continued to increase with time. Pretreatment injections (s.c.) of dm-PGE2 (3 and 30 μg/kg), papaverine (100 mg/kg), and atropine (1 mg/kg) protected the surface cells against stress-induced (1 h) damage, and inhibited visible lesion formation after 4 h stress. Timoprazole (30 mg/kg s.c.) did not protect the surface cells, but did markedly inhibit visible lesion formation. DmPGE2, papaverine, and atropine, but not timoprazole, inhibited stress-induced increases in gastric contractions. DmPGE2, timoprazole, and atropine, but not papaverine, inhibited acid secretion in stress conditions. These results indicated that stress induced damage to the gastric mucosa within 1 h due to increased gastric contractions, and the surface epithelial cell damage developed into macroscopically visible lesions in the presence of acid, and that dmPGE2 protected the surface epithelium against stress-induced damage probably by inhibiting gastric contractions.