Kobayashi K, Arakawa T, Nakamura H, Chono S, Yamada H, Satoh H, Ono T
Tohoku J Exp Med. 1983 Jun;140(2):181-5. doi: 10.1620/tjem.140.181.
The level of endogenous prostacyclin (PGI2), prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) in rat gastric mucosa was determined by radioimmunoassay to examine whether gefarnate, an antiulcer agent, maintained the endogenous prostaglandin (PG) level in rats subjected to water-immersion stress. Seven-hr immersion induced gastric lesions and a marked reduction in PGI2 and PGE2. When gefarnate was injected subcutaneously before stress exposure, the mean ulcer index was reduced and the PGI2 and PGE2 levels were maintained. Our results suggest that the reduction of endogenous PGI2 and PGE2 is a major factor in water-immersion-induced ulcers in rats, and that gefarnate inhibits this ulcer formation by inhibiting a reduction in those PGs induced by water-immersion stress.
采用放射免疫分析法测定大鼠胃黏膜中内源性前列环素(PGI2)、前列腺素E2(PGE2)和血栓素A2(TXA2)的水平,以研究抗溃疡药吉法酯是否能维持水浸应激大鼠体内内源性前列腺素(PG)水平。7小时的水浸可导致胃损伤以及PGI2和PGE2显著降低。在应激暴露前皮下注射吉法酯,平均溃疡指数降低,PGI2和PGE2水平得以维持。我们的结果表明,内源性PGI2和PGE2的降低是大鼠水浸诱导溃疡的主要因素,且吉法酯通过抑制水浸应激诱导的PGs降低来抑制这种溃疡形成。