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胃酸和胰多肽对改良假饲的反应。迷走神经干切断术和壁细胞迷走神经切断术的影响。

Gastric acid and pancreatic polypeptide responses to modified sham feeding. Effects of truncal and parietal cell vagotomy.

作者信息

Konturek S J, Popiela T, Słowiaczek M, Bielański W

出版信息

Gut. 1987 Mar;28(3):280-6. doi: 10.1136/gut.28.3.280.

Abstract

The effects of truncal vagotomy and parietal cell vagotomy on gastric acid secretion and plasma gastrin and pancreatic polypeptide release were studied in 28 duodenal ulcer patients under basal conditions and after modified sham feeding and infusion of pentagastrin (2 micrograms/kg/h). Before vagotomy gastric acid output in response to modified sham feeding was significantly higher than basal acid secretion in all subjects tested and reached about 45% of the pentagastrin maximum. No difference in the increase in acid response, or in the pancreatic polypeptide response to modified sham feeding was found between patients with high and low basal secretion. Plasma gastrin concentration was unaltered by modified sham feeding before and after truncal vagotomy or parietal cell vagotomy, although after vagotomy it tended to reach higher values than before this procedure. After truncal vagotomy, basal pancreatic polypeptide concentration was decreased and modified sham feeding-induced pancreatic polypeptide increment was completely eliminated. Four weeks after parietal cell vagotomy, the modified sham feeding-induced increment in plasma pancreatic polypeptide was significantly decreased and observed only in seven of 12 patients. Four to five years after parietal cell vagotomy all subjects responded to modified sham feeding with pancreatic polypeptide increment similar to that before vagotomy and in three of 12 patients acid response to modified sham feeding was seen. This study indicates that truncal vagotomy eliminates gastric acid and plasma pancreatic polypeptide responses to vagal excitation while parietal cell vagotomy abolishes gastric acid response and reduces temporarily the pancreatic polypeptide response to modified sham feeding (possibly because of transient impairment of the vagal innervation of the pancreas). (2) A high ratio of basal to maximal acid output in non-operated duodenal ulcer patients is not associated with a low acid response to modified sham feeding, nor with a high pancreatic polypeptide concentration, and (3) Restitution of the pancreatic polypeptide response to modified sham feeding five years after parietal cell vagotomy does not indication ineffective denervation of the parietal cells.

摘要

在28例十二指肠溃疡患者中,研究了迷走神经干切断术和壁细胞迷走神经切断术对基础状态下以及改良假饲和注射五肽胃泌素(2微克/千克/小时)后胃酸分泌、血浆胃泌素及胰多肽释放的影响。在迷走神经切断术前,所有受试对象对改良假饲的胃酸分泌量显著高于基础胃酸分泌量,达到五肽胃泌素最大分泌量的约45%。基础分泌量高和低的患者之间,对改良假饲的胃酸分泌增加量或胰多肽反应没有差异。迷走神经干切断术或壁细胞迷走神经切断术前、后,改良假饲均未改变血浆胃泌素浓度,不过迷走神经切断术后其浓度往往比手术前更高。迷走神经干切断术后,基础胰多肽浓度降低,改良假饲诱导的胰多肽增加量完全消失。壁细胞迷走神经切断术后4周,改良假饲诱导的血浆胰多肽增加量显著减少,仅在12例患者中的7例观察到。壁细胞迷走神经切断术后4至5年,所有受试者对改良假饲的反应是胰多肽增加,与迷走神经切断术前相似,12例患者中有3例出现对改良假饲的胃酸反应。本研究表明,迷走神经干切断术消除了胃酸和血浆胰多肽对迷走神经兴奋的反应,而壁细胞迷走神经切断术消除了胃酸反应,并暂时降低了对改良假饲的胰多肽反应(可能是由于胰腺迷走神经支配的短暂受损)。(2)未手术的十二指肠溃疡患者基础胃酸分泌量与最大胃酸分泌量的高比值,与对改良假饲的低胃酸反应无关,也与高胰多肽浓度无关,并且(3)壁细胞迷走神经切断术后5年胰多肽对改良假饲反应的恢复并不表明壁细胞去神经支配无效。

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