Morris G P, Wallace J L, Harding P L
Can J Physiol Pharmacol. 1984 Sep;62(9):1065-9. doi: 10.1139/y84-178.
The effects of pretreatment with prostaglandin E2 (PGE2) on salicylate-induced gastric damage in the rat were studied with a gastric chamber model. Transmural potential difference (PD) and net potassium ion (K+) efflux were monitored as indices of gastric mucosal barrier integrity. Topical application of 20 mM salicylate for 10 min produced an abrupt drop in PD, an increase in net K+ flux, and the formation of hemorrhagic erosions covering approximately 24% of the glandular mucosa. Prior topical application of PGE2 at doses of 25, 75, and 300 micrograms/kg significantly reduced the extent of hemorrhagic erosions. However, PG pretreatment did not produce a reduction in the effects of topical salicylate on either PD or net K+ efflux. Rather, the drop in PD was initially accelerated and the net K+ efflux was increased by PGE2 pretreatment. Subsequently, in PGE2-pretreated mucosae, both parameters showed more rapid recovery toward control values. These results suggest that the mechanism of "cytoprotection" by PGE2 against salicylate-induced gastric damage is not a consequence of preservation of the gastric mucosal barrier.
采用胃腔模型研究了前列腺素E2（PGE2）预处理对大鼠水杨酸盐诱导的胃损伤的影响。监测跨膜电位差（PD）和净钾离子（K+）外流作为胃黏膜屏障完整性的指标。局部应用20 mM水杨酸盐10分钟导致PD突然下降、净K+通量增加，并形成覆盖约24%腺性黏膜的出血性糜烂。预先局部应用剂量为25、75和300微克/千克的PGE2可显著降低出血性糜烂的程度。然而，PG预处理并未降低局部应用水杨酸盐对PD或净K+外流的影响。相反，PGE2预处理使PD的下降最初加速，净K+外流增加。随后，在PGE2预处理的黏膜中，这两个参数均显示出更快地恢复到对照值。这些结果表明，PGE2对水杨酸盐诱导的胃损伤的“细胞保护”机制不是胃黏膜屏障得以保留的结果。
