组胺和应激对胃溃疡形成过程中胃黏膜钙离子含量的影响。

Effect of histamine and stress on the gastric mucosal Ca2+ content during the development of gastric ulcers.

作者信息

Grechishkin L L, Riethling K, Zelck U, Karnstedt U

出版信息

Agents Actions. 1979 Dec;9(5-6):445-9. doi: 10.1007/BF01968108.

DOI:10.1007/BF01968108

Abstract

The influence of histamine, its triazole derivative (3-beta-aminoethyl-1,2,4-triazole) and immobilization stress on the gastric mucosal Ca2+ content during the development of gastric ulcers in guinea pigs and rats was investigated. A considerable fall in the concentration of Ca2+ in gastric tissues of guinea pigs after administration of histamine 0.25 mg/kg, down to 80% (8.0 mumol/g), its derivative (1 mg/kg) to 72% (7.2 mucol/g) and stress to 76% (7.6 mumol/g) was recorded by atomic absorption-spectrophotometric techniques, while the calcium level in the controls stood at 9.9 mumole/g. Similar changes (90-65%) were seen in the blood plasma. In rats, the Ca2+-decreasing effects of stress ran closely parallel with increasing ulceration, and depended on the duration of stress. The immobilization of rats evoked a slight rise in the Na+ content of the gastric tissues. After 4 h immobilization, the tissue concentration of Na+ was increased to 116% of control levels. Cimetidine (100 mumol kg-1 more than 50% inhibited the development of gastric ulcers and prevented the change in Ca2+ concentration ions. Thus, the data suggest that Ca2+ ions take part not only in the regulation of secretion, but also in stress tissue dystrophy.

摘要

研究了组胺、其噻唑衍生物（3-β-氨乙基-1,2,4-噻唑）和固定应激对豚鼠和大鼠胃溃疡形成过程中胃黏膜Ca2+含量的影响。通过原子吸收分光光度技术记录到，给予组胺0.25mg/kg后，豚鼠胃组织中Ca2+浓度显著下降至80%（8.0μmol/g），给予其衍生物（1mg/kg）后降至72%（7.2μmol/g），应激后降至76%（7.6μmol/g），而对照组的钙水平为9.9μmol/g。血浆中也出现了类似的变化（90%-65%）。在大鼠中，应激导致的Ca2+降低效应与溃疡形成的增加密切相关，并取决于应激的持续时间。大鼠固定后胃组织中Na+含量略有升高。固定4小时后，组织中Na+浓度增加至对照水平的116%。西咪替丁（100μmol/kg）可抑制胃溃疡的形成超过50%，并防止Ca2+浓度离子的变化。因此，数据表明Ca2+离子不仅参与分泌调节，还参与应激组织营养不良。