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胃泌素瘤细胞胃泌素释放的β-肾上腺素能调节

Beta-adrenergic regulation of gastrin release from gastrinoma cells.

作者信息

Sakamoto T, Miyata M, Hamaji M, Sakaguchi H, Tanaka Y, Hashimoto T, Kawashima Y

机构信息

First Department of Surgery, Osaka University Medical School, Japan.

出版信息

Surgery. 1990 Mar;107(3):282-8.

PMID:2155479
Abstract

The effect of epinephrine on the plasma gastrin level was investigated in three patients with Zollinger-Ellison syndrome (ZES) and in 14 normal subjects. Two ZES patients had undergone total gastrectomy, and the third had undergone subtotal gastrectomy before our study. A significant increase in plasma gastrin, from 23 +/- 5 pg/ml to 53 +/- 20 pg/ml, in response to intravenous epinephrine (40 ng/kg.min), was observed in the normal subjects. This response was completely abolished by beta-blockade. In the ZES patients, epinephrine (40 ng/kg.min) also resulted in an increase in the plasma concentration of gastrin. The basal and maximum concentrations of gastrin were 580 and 1680 pg/ml in patient 1, 145000 and 320000 pg/ml in patient 2, and 200 and 1800 pg/ml in patient 3, respectively. beta-Adrenergic blockade suppressed the epinephrine-stimulated gastrin release in these patients as well. Graded intravenous doses of epinephrine given to the ZES patients resulted in elevation of the plasma gastrin in a dose-dependent manner. Insulin hypoglycemia caused an increase in both plasma epinephrine and plasma gastrin in ZES patients and normal subjects. A significant correlation between plasma gastrin and epinephrine during insulin hypoglycemia was observed in both groups. Exercise, with use of a bicycle ergometer, resulted in an increase in plasma epinephrine. An increase in plasma gastrin with exercise was observed in the ZES patients, and this was also suppressed by beta-blockade. The results suggest that gastrinoma cells, like normal G cells, are equipped with beta-adrenergic receptors that regulate gastrin release.

摘要

研究了肾上腺素对3例佐林格-埃利森综合征(ZES)患者和14名正常受试者血浆胃泌素水平的影响。2例ZES患者在我们研究前已接受全胃切除术,第3例接受了胃次全切除术。正常受试者静脉注射肾上腺素(40 ng/kg·min)后,血浆胃泌素显著升高,从23±5 pg/ml升至53±20 pg/ml。β受体阻滞剂可完全消除这种反应。在ZES患者中,肾上腺素(40 ng/kg·min)也导致胃泌素血浆浓度升高。患者1胃泌素的基础浓度和最高浓度分别为580和1680 pg/ml,患者2为145000和320000 pg/ml,患者3为200和1800 pg/ml。β肾上腺素能阻滞剂也抑制了这些患者中肾上腺素刺激的胃泌素释放。给ZES患者静脉注射不同剂量的肾上腺素导致血浆胃泌素呈剂量依赖性升高。胰岛素低血糖症导致ZES患者和正常受试者的血浆肾上腺素和血浆胃泌素均升高。两组在胰岛素低血糖期间血浆胃泌素和肾上腺素之间均观察到显著相关性。使用自行车测力计进行运动导致血浆肾上腺素升高。ZES患者运动后血浆胃泌素升高,且也被β受体阻滞剂抑制。结果表明,胃泌素瘤细胞与正常G细胞一样,具有调节胃泌素释放的β肾上腺素能受体。

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Beta-adrenergic regulation of gastrin release from gastrinoma cells.胃泌素瘤细胞胃泌素释放的β-肾上腺素能调节
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