Histochemical and ultrastructural alterations of the duodenum in acute hypoxia

L. Józsa, O. Szekely, A. Reffy

Research output: Contribution to journalArticle

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Abstract

Laboratory animals were kept for 2, 8 and 16 hr in a pressure chamber, the air of which contained 8% O2 and 92% N2. Histochemical and ultrastructural examinations revealed the following duodenal alterations: The alkaline phosphatase activity of the epithelium and glandular epithelium showed no alteration; the acid phosphatase activity was slightly increased in hypoxia. The succinic dehydrogenase and cytochrome C oxidase activities of the glandular epithelium showed a marked decrease. Two hours of hypoxia led to destruction of the microvillous epithelium. Prolonged hypoxia resulted in the destruction of the microvilli as well as of the cuticula. Hypoxia of short duration had no damaging effect on glandular epithelial cells. After 8 to 16 hr of hypoxia, glandular secretion was reduced and the epithelial cells were evacuated. From the findings of the present investigation it is concluded that the decrease in the production of protective intestinal juice, due to the damaging effect of hypoxia on the epithelium and glandular epithelium as well as on the mitochondria, and the increase in the absorption of the intestinal content should be considered responsible for the additional damages to the intestinal epithelium.

Original languageEnglish
Pages (from-to)168-179
Number of pages12
JournalZeitschrift fur Experimentelle Chirurgie
Volume9
Issue number3
Publication statusPublished - 1976

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Duodenum
Epithelium
Epithelial Cells
Air Pressure
Gastrointestinal Contents
Succinate Dehydrogenase
Laboratory Animals
Electron Transport Complex IV
Intestinal Mucosa
Microvilli
Acid Phosphatase
Alkaline Phosphatase
Hypoxia
Mitochondria

ASJC Scopus subject areas

  • Medicine(all)

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Histochemical and ultrastructural alterations of the duodenum in acute hypoxia. / Józsa, L.; Szekely, O.; Reffy, A.

In: Zeitschrift fur Experimentelle Chirurgie, Vol. 9, No. 3, 1976, p. 168-179.

Research output: Contribution to journalArticle

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