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Effect of hypoxia on the connective tissue of aorta and skin in rabbits Biochemical and morphological studies

  • P. Helin
    Affiliations
    Medical Department C, Gentofte Hospital, Connective Tissue Research Laboratories, Department of Dermatology, Rigshospital and Laboratory of Cyto- and Histochemistry, Anatomy Department A, University of Copenhagen, Copenhagen, Denmark
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  • C. Garbarsch
    Affiliations
    Medical Department C, Gentofte Hospital, Connective Tissue Research Laboratories, Department of Dermatology, Rigshospital and Laboratory of Cyto- and Histochemistry, Anatomy Department A, University of Copenhagen, Copenhagen, Denmark
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  • T. Mørk Hansen
    Affiliations
    Medical Department C, Gentofte Hospital, Connective Tissue Research Laboratories, Department of Dermatology, Rigshospital and Laboratory of Cyto- and Histochemistry, Anatomy Department A, University of Copenhagen, Copenhagen, Denmark
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  • G. Helin
    Affiliations
    Medical Department C, Gentofte Hospital, Connective Tissue Research Laboratories, Department of Dermatology, Rigshospital and Laboratory of Cyto- and Histochemistry, Anatomy Department A, University of Copenhagen, Copenhagen, Denmark
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  • B. Kofod
    Affiliations
    Medical Department C, Gentofte Hospital, Connective Tissue Research Laboratories, Department of Dermatology, Rigshospital and Laboratory of Cyto- and Histochemistry, Anatomy Department A, University of Copenhagen, Copenhagen, Denmark
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  • I. Lorenzen
    Correspondence
    Request for reprints to: 1. Lorenzen, M.D., Gentofte Hospital, Medical Department C, DK-2900 Hellerup/Copenhagen, Denmark.
    Affiliations
    Medical Department C, Gentofte Hospital, Connective Tissue Research Laboratories, Department of Dermatology, Rigshospital and Laboratory of Cyto- and Histochemistry, Anatomy Department A, University of Copenhagen, Copenhagen, Denmark
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      Abstract

      Male albino rabbits were exposed to a systemic hypoxia of 10% oxygen for 3 and 30 days. The effects of the hypoxia on the undamaged aortas as well as on aortas subjected to a single mechanical dilatation injury were studied. The aortas were analysed with respect to gross and microscopic changes as well as to biochemical changes in glycosaminoglycans, hydroxyproline, permeability to 1251-albumin and dry weight. Furthermore, the glycosaminoglycans and hydroxyproline fractions of the skin were investigated. Hypoxia per se induced no gross or microscopic alterations in aorta. Neither did hypoxia influence the gross arteriosclerotic changes nor the microscopic changes induced by the dilatation injury. The biochemical effects of the hypoxia on aorta depended upon two factors: the duration of the hypoxia and the presence of a prior vascular damage. Short-term hypoxia increased the aortic content of dermatan sulphate as well as the synthesis of chondroitin-4/6-sulphate and of the dermatan sulphate-heparan sulphate fraction in undamaged aortas. This effect could not be detected in the presence of a recent vascular damage. In undamaged aortas long-term exposure to hypoxia decreased the aortic content of chondroitin-4/6-sulphate and inhibited the synthesis of the heparan sulphate-dermatan sulphate fraction. These alterations were not observed in the presence of aortic injury prior to the hypoxia. In undamaged as well as damaged aortas long-term hypoxia decreased the content of hexosamine and hydroxyproline, the total dry weight of the aortas as well as the inner surface areas. The changes in the glycosaminoglycans of the skin in animals exposed to hypoxia were rather similar to those of the undamaged aortas. Long term hypoxia prevented the weight loss dependent decrease in the 0.14 M salt soluble hydroxyproline fraction of the skin. No changes in the permeability to 1251-albumin could be detected. The reported alterations in the aortic glycosaminoglycans and hydroxyproline following hypoxia may be of pathogenetic significance in arteriosclerosis by influencing the transport of lipoproteins in the arterial wall and by lowering the resistance of the arterial wall to injury induced by the haemodynamic strain.

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