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胃酸对幽门结扎反应的机制:肾切除术的影响。

Mechanism of gastric acid response to pylorus ligation: effects of nephrectomy.

作者信息

Vallgren S, El Munshid H A, Hedenbro J, Rehfeld J F, Håkanson R

出版信息

Scand J Gastroenterol. 1983 May;18(4):491-6. doi: 10.3109/00365528309181628.

DOI:10.3109/00365528309181628
PMID:6669925
Abstract

In the rat nephrectomy raises the serum gastrin concentration but makes the parietal cells refractory to gastrin. Pylorus ligation stimulates the gastric acid output by a long vago-vagal reflex in innervated animals and by an intramural reflex in chronically vagotomized animals. Nephrectomy reduced the acid response to pylorus ligation in vagally intact rats but enhanced it in vagotomized rats. The acid response to pylorus ligation in all the experimental groups was inhibited by a muscarinic blocker, atropine, and by an H2-antagonist, metiamide. The serum gastrin concentration was raised by nephrectomy and by vagal denervation. Histamine mobilization from gastric endocrine cells is reflected in the activity of gastric histidine decarboxylase. The enzyme activity in pylorus-ligated innervated rats was raised by pentagastrin, atropine, and metiamide. In nephrectomized rats the basal enzyme activity was high, and it was raised further, slightly but significantly, by pentagastrin. The basal enzyme activity in pylorus-ligated rats was also quite high after vagotomy, and it was raised further by pentagastrin. After vagotomy + nephrectomy the basal enzyme activity was very high; it was not raised further by pentagastrin. It appears that both vago-vagal and intramural reflexes involve a cholinergic and a histaminergic pathway, that gastrin is not important for the neurally mediated acid response elicited by pylorus ligation, and that the postulated histaminergic pathway does not involve histamine derived from the gastric endocrine-like cells.

摘要

在大鼠中,肾切除会提高血清胃泌素浓度,但会使壁细胞对胃泌素产生耐受。幽门结扎在有神经支配的动物中通过长迷走 - 迷走反射刺激胃酸分泌,在长期迷走神经切断的动物中通过壁内反射刺激胃酸分泌。肾切除降低了迷走神经完整大鼠对幽门结扎的酸反应,但增强了迷走神经切断大鼠的酸反应。所有实验组中,对幽门结扎的酸反应均受到毒蕈碱阻断剂阿托品和H2拮抗剂甲硫米特的抑制。肾切除和迷走神经切断均会提高血清胃泌素浓度。胃内分泌细胞中组胺的释放反映在胃组氨酸脱羧酶的活性上。在幽门结扎的有神经支配的大鼠中,五肽胃泌素、阿托品和甲硫米特会提高该酶的活性。在肾切除的大鼠中,基础酶活性较高,五肽胃泌素会使其进一步轻微但显著升高。在迷走神经切断后的幽门结扎大鼠中,基础酶活性也相当高,五肽胃泌素会使其进一步升高。在迷走神经切断 + 肾切除后,基础酶活性非常高;五肽胃泌素不会使其进一步升高。似乎迷走 - 迷走反射和壁内反射均涉及胆碱能和组胺能途径,胃泌素对幽门结扎引起的神经介导的酸反应并不重要,并且假定的组胺能途径并不涉及源自胃内分泌样细胞的组胺。

相似文献

1
Mechanism of gastric acid response to pylorus ligation: effects of nephrectomy.胃酸对幽门结扎反应的机制:肾切除术的影响。
Scand J Gastroenterol. 1983 May;18(4):491-6. doi: 10.3109/00365528309181628.
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Mechanisms of gastric acid secretion after pylorus and oesophagus ligation in the rat.大鼠幽门和食管结扎后胃酸分泌的机制
J Physiol. 1980 Aug;305:139-49. doi: 10.1113/jphysiol.1980.sp013355.
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Gastric acid response to pylorus ligation in rats: is gastrin or histamine involved?大鼠幽门结扎后胃酸的反应:胃泌素或组胺是否参与其中?
J Physiol. 1982 Feb;323:145-56. doi: 10.1113/jphysiol.1982.sp014065.
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Importance of the kidneys for gastrin elimination and gastric function.肾脏对胃泌素清除及胃功能的重要性。
J Physiol. 1980 Feb;299:157-71. doi: 10.1113/jphysiol.1980.sp013117.
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Mechanism of hypergastrinaemia after nephrectomy in the rat.大鼠肾切除术后高胃泌素血症的机制。
Acta Physiol Scand. 1985 Nov;125(3):383-8. doi: 10.1111/j.1748-1716.1985.tb07733.x.
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Rat stomach enterochromaffin-like cells are not stimulated by pylorus ligation. A biochemical and ultrastructural study.
Scand J Gastroenterol. 1996 Jan;31(1):31-7. doi: 10.3109/00365529609031623.
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Suppression of rat stomach histidine decarboxylase activity by histamine: H2-receptor-mediated feed-back.组胺对大鼠胃组织中组氨酸脱羧酶活性的抑制作用:H2受体介导的反馈调节。
J Physiol. 1977 Aug;269(3):643-67. doi: 10.1113/jphysiol.1977.sp011920.
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Comparative evaluation of the role of endogenous gastrin in basal acid secretion in conscious rats provided with chronic fistula and pylorus ligation.对患有慢性瘘管和幽门结扎的清醒大鼠内源性胃泌素在基础胃酸分泌中的作用进行比较评估。
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Correlation between serum gastrin concentration and rat stomach histidine decarboxylase activity.血清胃泌素浓度与大鼠胃组织组氨酸脱羧酶活性之间的相关性。
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Anaesthetic agents suppress basal and stimulated gastric acid secretion. Are intramural neurons involved?麻醉剂会抑制基础胃酸分泌和刺激后的胃酸分泌。壁内神经元参与其中吗?
Scand J Gastroenterol. 1991 Nov;26(11):1200-4. doi: 10.3109/00365529108998614.

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