Pharmacology of Neurogenic Dystrophies Produced by Stress

Zavodskaya, I. S.

doi:10.1016/b978-0-08-023768-8.50255-3

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“…Anichkov and his colleagues showed that stress by means of fl-adreno-receptors and the adenylyl cyclase system at first stimulated energy processes, and after that exhausted tissue energy resources and thus developed mucosal damage in the stomach [26,27]. The histamine-H2-receptor system also acts in this direction.…”

Section: Discussionmentioning

confidence: 97%

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

et al. 1979

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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.

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Section: Discussionmentioning

confidence: 97%