Cheung L Y
Prostaglandins. 1981;21 Suppl:125-9. doi: 10.1016/0090-6980(81)90128-3.
This study was designed to evaluate whether stimulation of mucus and alkaline secretion by topical 16,16-dimethyl prostaglandin E2 (dmPGE2) would protect gastric mucosa against aspirin-induced disruption of permeability barrier to lumina acid. A chambered segment of canine fundic stomach with intact vascular supply was partitioned into two compartments. One was pretreated with topical dmPGE2 (25 micrograms/15 ml isotonic acid) and the other served as control. Topical dmPGE2 resulted in 1) mucus release as evidenced by gross and microscopic examinations, 2) luminal volume gain from 0.05 +/- 0.01 to 1.05 +/- 0.30 ml/15 min (p less than 0.01) and 3) an increase in Na+ efflux from 9 +/- 4 to 165 +/- 20 muEq/15 min (p less than 0.001). These effects of dmPGE2 did not protect the gastric mucosa against disruption of permeability barrier induced by 20 mM aspirin, which resulted in a similar amount of H+ back-diffusion in dmPGE2-treated mucosa (8 +/- 7 to 129 +/- 8 muEq/15 min, p less than 0.001) and in control mucosa (from 5 +/- 7 to 118 +/- 24 muEq/15 min, p less than 0.001). Also there was no significant difference in the degree of reduction in mucosal potential difference between dmPGE2-treated mucosa (from 60 +/- 4 to 34 +/- 2 -mV p less than 0.01) and control mucosa (from 58 +/- 4 to 36 +/- 3 -mV p less than 0.001).
本研究旨在评估局部应用16,16-二甲基前列腺素E2(dmPGE2)刺激黏液和碱性分泌是否能保护胃黏膜免受阿司匹林诱导的对腔内酸通透性屏障的破坏。将具有完整血液供应的犬胃底部带腔节段分为两个隔室。一个隔室用局部dmPGE2(25微克/15毫升等渗酸)预处理,另一个作为对照。局部应用dmPGE2导致:1)通过大体和显微镜检查证明有黏液释放;2)管腔容积从0.05±0.01增加至1.05±0.30毫升/15分钟(p<0.01);3)钠外流从9±4增加至165±20微当量/15分钟(p<0.001)。dmPGE2的这些作用未能保护胃黏膜免受20毫摩尔阿司匹林诱导的通透性屏障破坏,阿司匹林导致dmPGE2处理的黏膜(从8±7至129±8微当量/15分钟,p<0.001)和对照黏膜(从5±7至118±24微当量/15分钟,p<0.001)中类似量的氢离子反向扩散。此外,dmPGE2处理的黏膜(从60±4至34±2毫伏,p<0.01)和对照黏膜(从58±4至36±3毫伏,p<0.001)之间黏膜电位差降低程度无显著差异。