慢性硬膜下血腫のprostaglandin動態とその意義について

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概要

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• The kinetics of prostaglandin (PG) in hematomas and circulating blood plasma was explored in 29 cases of chronic subdural hematoma (31 hematomas), divided into four groups according to the density of hematoma on computed tomography scanning, i.e., low density (L), isodensity (I), high density (H), and combined density (C). The study disclosed the following: 1) PG E levels of hematoma fluid were high in Groups H and I and low in Group L. The plasma level of PG E was found elevated in Groups C and I, and generally was less variable. 2) The 6-keto-PG F_<1α> content of hematoma fluid was slightly increased in Groups H and I, but showed no variation in Groups L and C. 3) Thromboxane B_2 (TX B_2) was noted to be increased in both hematoma fluid and circulating plasma in all groups. 4) Hematomas of Group L showed high values of TX B_2/6-keto-PG F_<1α> ratio. Plasma values of this parameter were heightened in all groups. 5) The plasma level of PG F_<2α> showed no noticeable variation, while the hematoma fluid content of PG F_<2α> was increased in all groups, especially markedly in Group I. 6) Elevated serum estrogen levels, notably of estrone, were observed in all groups. In Groups C, I, and H, serum estrogens rose in parallel with the hematoma fluid level of PG F_<2α>. 7) The leukocyte fraction from hematoma fluid in Groups I, C, and H was found to contain a high percentage of eosinophils. These facts suggest that in chronic subdural hematoma there occurs generalized activation of the blood clotting system with increased local vasoconstrictive capacity at the site of hematoma formation. These biological responses were heightened in Groups I, C, and H, while less pronounced in Group L. The study also revealed that there was hyperactivity of the platelet aggregation-inhibiting system at the site of hematoma in Groups I and H. PG was thus demonstrated to play a role in the antagonism between the systemically increased capacity of platelet aggregation and the enhanced platelet aggregation-inhibiting activity at the affected locality, and thereby to participate in the formation and healing of a hematoma.

• 日本脳神経外科学会の論文
• 1987-06-15

著者

• 松森 邦昭

  国立相模原病院 脳神経外科

• 吉岡 美知子

  Special Reference Laboratory

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