第三脑室注射组胺及其受体激动剂对五肽促胃液素诱导的大鼠胃酸分泌的影响

本文报道第三脑室注射组胺(0.25—2.0μg/5μl)对五肽促胃液素诱导的胃酸分泌的双重影响。雄性Wistar大鼠,重200—300g,戊巴比妥钠腹腔麻醉。用37℃生理盐水通过恒流泵进行连续胃灌流。在静脉恒速灌注五肽促胃液素(7.5μg/kg·h)的基础上,第三脑室注射组胺(0.25μg/5μl)或H_1受体激动剂2-Pyridylethylamine(PEA,10μg/5μl),10min后总酸排出量即开始减少,90min仍未恢复。组胺剂量增至1.0μg或2.0μg时,出现双重效应。部份动物(分别占73％或50％)胃酸分泌减少,另一部分动物(27％或50％)胃酸分泌增多。H_2受体激动剂dimaprit(10μg/5μl)或impromidine(0.1μg/5μl)对胃酸分泌无明显影响。苯海拉明(16μg/0.2ml或32μg/0.2ml,i.m.)预处理可分别取消组胺和PEA的抑胃酸效应。这些结果提示:脑内组胺可能参与胃酸分泌中枢调节。其抑制效应似通过H_1受体介导;双重效应的机制有待进一步研究。     

组胺H1受体激动剂PEA抑制胃酸分泌效庆的中枢机制

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灌流。第三脑室给药,观察其对五肽促胃液素（１６０μｇ／ｋｇｓ．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１０μｇＰＥＡ的中枢抑酸效应;（２）分别脑室给予ＣＲＦ（１．０和２．０μｇ）β－内啡肽（０．９４和１．２５     

第三脑室注射组织胺增强五肽促胃液素诱导的胃酸分泌的作用机制

本文探讨中枢组织胺增强胃酸分泌的作用机制。雄性ＳＤ大鼠重２００－３００ｇ,用３７℃生理盐水做恒速,连续胃灌流。膈下迷走神经切除后,观察第三脑室或外周给药对五肽促胃激素诱导的胃酸分泌及对血交涉以质酮水平的影响。结果如下：１．第三脑室注射１．０μｇ组织胺增强Ｇ－５诱导的胃酸分泌,这作用可为预先肌肉注射苯海拉明８．０μｇ听阻断。２．脑注射促肾上腺皮质激素释放因子增强因酸分泌,且呈量效关系。３．脑室注射组     

脑室注射组胺抑制大鼠胃酸分泌的外周机制

本文分析了第三脑室注射组胺（HA）抑制胃酸分泌效应的外周过程。雄性SD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灌流。用注射器泵静脉每小时给药,观察其对五肽促胃液素（10μg/kg,iv）诱导的胃酸分泌的影响。结果如下：（1）切除双侧膈下迷走神经可阻断HA（1μg,icv）的中枢抑酸效应;（2）预先静脉注射硫酸阿托品［0.05mg／（kg·100min）］可阻断HA的中枢抑酸效应;（3）预先静脉注射生长抑素拮抗剂[2～4μg/（kg·100min）],可剂量依赖性地拮抗HA的中枢抑酸效应。结果提示：HA的中枢抑酸效应由迷走神经传出,可能通过乙酰胆碱M受体及引起生长抑素释放实现。     

组胺H_1受体激动剂PEA抑制胃酸分泌效应的中枢机制

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。     

第三脑室注射组胺及其受体激动剂对五肽促胃液素诱导...

The present study shows the dual effects of intraventricularly injected histamine (0.25-2.0 micrograms/5 microliters) on pentagastrin-induced gastric acid secretion. Male Wistar rats weighing 200-300 g were anesthetized with intraperitoneal sodium pentobarbital. Gastric acid was continuously washed out with 37 degrees C saline solution by means of a perfusion pump. On the background of continuous intravenous infusion of pentagastrin [7.5 micrograms/(kg.h),] histamine (0.25 microgram/5 microliters) or 2-pyridylethylamine (PEA, 10 micrograms/5 microliters), a H1-receptor agonist, was injected into the third ventricle through a chronically implanted canula. The acid output decreased 10 min after injection and did not recover at 90 min. When the dose of histamine was increased to 1.0 micrograms or 2.0 micrograms, dual effects appeared. The acid output decreased respectively in 73% or 50% of the animals, while in the rest 27% and 50% of the animals, the acid output increased. H2-receptor agonist dimaprit (10 micrograms/5 microliters, i.c.v.) or impromidine (0.1 micrograms/5 microliters, i.c.v.) had no pronounced effect on pentagastrin-induced acid secretion. Pretreatment with diphenhydramine (16 micrograms/0.2 ml or 32 micrograms/0.2 ml, i.m.) abolished the inhibitory effect of histamine and PEA on acid secretion. These results suggest that histamine may be involved in the central regulation of gastric acid secretion, and the inhibitory effect may be mediated by H1-receptors in the brain. The mechanism underlying the production of the dual effects of histamine is unknown.     

脑室注射组胺H1受体激动剂对大鼠胃酸分泌的作用机制

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２００－３００ｇ,用３７（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