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本文分析了中枢注射ＰＥＡ抑制胃酸分泌效应的脑内过程。雄性Ｗｉｓｔａｒ大鼠，摘除双侧肾上腺，用３７℃的生理盐水通过恒流泵进行连续胃液流。第三脑室给药，观察其对五肽促胃液素（１６０μｇ／ｋｇ，ｓ．ｃ．）诱导的胃酸分泌的影响。结果如下：（１）预先脑室注射抗ＣＲＦ血清（２．５μｌ，１：２００００）可阻断１ＯμｇＰＥＡ的中枢抑酸效应；（２）分别脑室给予ＣＲＦ（１．０和２．０μｇ）和β－内啡肽（０．９４和１．２５μｇ）均明显抑制胃酸分泌；（３）预先注射纳洛酮（５．０μｇ，ｉ，ｃ．ｖ，）可取消ＣＲＦ（１．０μｇ）的中枢抑酸效应，而预先注射抗ＣＲＦ血清（２．５μｌ）对β－内啡肽（０．９４μｇ）的中枢抑酸效应无明显影响。结果提示：ＰＥＡ可能首先引起ＣＲＦ释放，后者再刺激内源性阿片肽释放，从而导致迷走介导的胃酸分泌抑制效应。
This article analyzes the central brain injection of PEA inhibition of gastric acid secretion in the brain process. Male Wistar rats, both sides of the adrenal removed, with 37 ℃ saline through a constant flow pump for continuous gastric flow. The third ventricle was dosed to observe its effect on gastric acid secretion induced by pentagastrin (160 μg / kg, s.c.). The results were as follows: (1) The preinventricular injection of anti-CRF serum (2.5μl, 1: 20000) blocked the central suppressive effect of 10μgPEA; (2) CRV (1.0 and 2.0μg) and β- Endorphins (0.94 and 1.25μg) significantly inhibited gastric acid secretion; (3) Pretreatment with naloxone (5.0μg, i, c.v, Effect, while pre-injection of anti-CRF serum (2.5 μl) had no significant effect on the central inhibitory effect of β-endorphin (0.94 μg). The results suggest that PEA may first cause release of CRF, which in turn stimulates the release of endogenous opioid peptides, leading to a vagal-mediated inhibition of gastric acid secretion.