【摘要】 本文对中枢注射PEA抑制胃酸分泌的作用机制进行分析。雄性Wistar大鼠,重200—300 g,用37C生理盐水通过恒流泵进行连续胃灌流。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）预先注射纳洛酮2.5μg可阻断10μgPEA的中枢抑酸效应;（2）双侧膈下迷走神经切除可翻转PEA（5—20μg）的抑酸效应,且有量效关系;双侧肾上腺摘除对PEA中枢抑酸效应无明显影响:（3）预先注射抗CRF血清（1:20 000,2.5μl）或摘除双侧肾上腺均可取消去迷走后PEA（10μg）的兴奋效应;（4）脑室注射10μg PEA对去迷走后大鼠基础酸分泌无明显影响。结果提示:组胺H₁受体参与胃酸分泌中枢调节的抑制和兴奋机制。其传出途径可能分别与迷走神经和下丘脑-垂体-肾上腺轴有关。更多还原

【Abstract】 The present experiment is undertaken to study the mechanism of the inhibitory ef-fect of 2--pyridylethylamine （PEA, i. c. v.） on the gastric acid secretion. Gastric acidwas continuously washed out with 37℃ saline by means of a perfusion pump in Wis-tar rats weighing 200--300 g. Drugs were injected into the third ventricle to examinethe effect on pentagastrin--induced （160 μg/kg, s. c. ） gastric acid secretion. The re-sults were as follows: （1） Pretreatment with naloxone （2.5 μg, i. c. v.） blocked theinhibitory effect of PEA （10 μg,i. c. v.） on gastric acid secretion. （2 ） The inhibitoryeffect of PEA （5--20 μg, i. c. v. ） was turned into an excitatory effect after suodi-aphragmatic vagotomy in a dose--dependent manner, but not changed by bilateral a-drenalectomy. （3） In vagotomized rats, pretreatment with CRF--antiserum （1:20000, 2.5 μl, i. c. v. ） or bilateral adrenalectomy abolished the excitatory effect ofPEA （10 μg, i. c. v. ）. （4） PEA （10 μg, i. c. v. ） did not change the basal gastricacid secretion in vagotomized rats. These results suggest that histamine H₁--receptor inbrain may be involved in both the inhibitory and excitatory regulation of gastric acidsecretion mediated by vagus nerve and the hypothalamus--pituitary--adrenal axis.更多还原