Journal of Okayama Medical Association
Published by Okayama Medical Association

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高原氏病に出現する口腔壊疽についての実験的研究 第1編 肺炎双球菌により惹起された家鴨口蓋粘膜病変の組織学的研究

三谷 恭夫 岡山大学医学部耳鼻咽喉科学教室
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抄録
In acatalasemia we often encounter specific oral gangrene called Takahara's disease. With the purpose to elucidate the causative factor of this gangrene, ducks having only a trace amount of catalase in their blood or plalate tissue were used as experimental animals. Diplococcus pneumoniae (Type Ⅱ) is known to generate hydrogen peroxide and contains little or no catalatic substance in itself. By suspending this Diplococcus pneumoniae in isotonic saline solution of 0.75% glucose, this suspension was injected under the mucous membrane of the duck palate. Then histopathological investigations and macroscopical observations were carried out at certain intervals after the injection. The results obtained were as follows. 1) Macroscopically, 24 hours after injection there appeared whitish coat and slight reddening and swelling surrounding the coat, and 72 hours after injection gangrene resembling the one observable in acatalasemia cases appeared. 2) Experimental histopathological study showed marked changes in blood vessel wall, In contrast, pathological changes of muscles and glands were hardly observed. Now we hold such hypotheses proposed by Kaziro or Takahara that dysfunction of the so-called respiratory enzyme group or oxygen deficiency due to methemoglobin-formation are the causative factors of this disease. From these results, it is assumed that the macroscopical and histopathological changes in duck palate resembling the findings observed in acatalasemia cases were caused by the oxidative action of deposit of hydrogen peroxide generated by Diplococcus pneumoniae (Type Ⅱ). The action mechanism of hydrogen peroxide is not definitively clarified from these results. But it is certain that the circulatory disturbances brought about by the marked changes in blood vessel wall, especially the wall of arteries, seem to evoke definitively oral gangrene.
ISSN
0030-1558
NCID
AN00032489