Previous investigations have shown that brain
prostaglandin levels are transiently elevated following experimental fluid percussion
brain injury. Associated with these increased
prostaglandin levels there is
free radical production and abnormalities in cerebral arteriolar function. The purpose of this study was to determine whether experimental fluid percussion
brain injury in cats is associated with increased systemic levels of
prostaglandins and the
lipoxygenase product,
12-HETE. Blood samples were collected before and at various periods of time after 2.7 atm of fluid percussion
brain injury was produced in adult cats.
Prostaglandin and
12-HETE analysis was performed by radioimmunoassay after extraction of the plasma samples. The control levels for
6-keto-PGF1 alpha,
PGE2, and
12-HETE were 477 +/- 42, 2,372 +/- 431, and 13,328 +/- 1,769 pg/ml, respectively. Following injury all three
eicosanoids reached peak plasma levels by 1-5 min after injury. The percentile increases for all
eicosanoids were similar and increased from 70 to 110%. The increases were sustained at up to 30 min postinjury and by 1 h after injury were at control levels. As in previous studies,
hypertension following injury was maximal by 1 min postinjury and blood pressure had returned to near normal levels by 5 min postinjury. These studies demonstrate prolonged systemic increases in
eicosanoids following injury. Since
free radical production and vascular damage occur concomitantly with
eicosanoid production, the prolonged increases in these products suggest that there is an attainable therapeutic window following injury during which administration of
free radical scavengers may decrease radical damage and reduce the consequences of injury.