Kinetics of prostaglandin and its significance in chronic subdural hematoma.

Abstract

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 V, isodensity (1), 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 I1 and generally was less variable. 2) The 6-keto-PG F1α content of hematoma fluid was slightly increased in Groups H and I, but showed no variation in Groups L and C. 3) Thromboxane B2 (TX B2) 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 B2/6-keto-PG F1α ratio. Plasma values of this parameter were heightened in all groups. 5) The plasma level of PG F2α showed no noticeable variation, while the hematoma fluid content of PG F2α 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 F2α. 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.