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緒言
末梢動脈疾患ことに所謂特発性脱疽の本態については,現在まで大部分の研究が罹患血管の病理組織学的見地から行なわれて来た。古くWiniwarter57)が動脈内膜炎説を唱えてから,Buerger8)9)の感染による血栓血管炎説を始めとして動脈硬化によるとするもの,Ratschow38),和田56)等のごとく,アレルギーにその成因を求めるもの,遺伝的因子によるとするもの,煙草に原因を求めるものなど非常に多くの説があるが,結局いまだにBuergerの古典的な血栓血管炎説の域を出ることなく,疾患の本態的病因は解明されるに至つていない。本症の血管変化および病因の追求に当つて,このように困難を伴う理由は,高橋59)も述べているごとく,本症の血管の病理組織学的所見が,疾患の時期的な諸相により異なつた複雑な様相を示し,また発病初期の新鮮材料を得がたいために二次的変化を観察していることが多いためと考えられる。従つて末梢動脈疾患の本態を考察するに当り,これを末梢血管の病理組織学的見地のみにより追求することは極めて困難なことであろう。
Histopathological observations on the stellate, thoracic and lumbar sympathetic ganglions obtained from 46 cases with peripheralarterial diseases including Buerger's disease, Raynaud's disease and arteriosclerosis obliterans were performed along with 37 controlcases. A new nerve staining method discribed by Holmes Pickett was applied, and the following conclusions were obtained.
1) Evrn normal ganglions reveal various Changes, and degeneration of ganglion cells to some extent is presumed to be normal.
2) Ganglions in the group of peripheral arterial diseases display more dense cellularity of nerve element than in control group. Ganglions of Raynaud's disease display the thickest density of ganglion cells.
3) Hydropic alteration is slightly noticed in the diseased group, while the alteration is more frequently and evidently noticed in control group.
4) Nuclei in ganglion cells in the diseased group show the author's type I and II with diffuse or homologous chromatin distribution and large diameter, while nuclei in control group show author's type II and III with uneven chromatin distribution or pyknosis. CuPC affinity is more prominent in the diseased group.
5) In general, degenerative changes in the diseased group are rather slight compared with that of control group. It is presumed that the ganglion cells in the formr are cytologically more active than the latter.
6) No significant relations were noticed between histological findings of the ganglions and duration of the diseases, sites of arterial obstrution and later sequelawe of sympathectomy.
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