Experimental Traumatic Brain Injury Elevates Brain Prostaglandin E-2 and Thromboxane B-2 Levels in Rats

Prostaglandin E-2 (PGE(2)) and thromboxane B-2 (TxB(2)) levels were measured in rats following experimental traumatic brain injury. Rats (n = 36) were prepared for fluid percussion brain injury under pentobarbital anesthesia. Twenty-four hours later, rats were lightly anesthetized using methoxyflurane, injured (2.3 atm), and killed 5 or 15 min later. Twelve of the rats died before and are not included in the analyses. The following groups were used for data analysis: group I (n = 6) were sham-injured rats prepared for injury but not injured: group II (n = 6) were injured and killed 5 min later; group III (n = 12) were injured and killed 15 min posttrauma. Thirty seconds prior to sacrifice by decapitation into liquid nitrogen, all rats were injected with indomethacin (3 mg/kg, intravenously [IV]) to prevent postmortem PG synthesis. After sacrifice, brains were removed, weighed, and homogenized in a small quantity of phosphate buffer with indomethacin (50 ug/ml). PGE(2) and TxB(2) levels were determined using double-label radioimmunoassays. Posttraumatic convulsions were observed in 5 of 12 rats in group III and these rats were analyzed separately. PGE(2) and TxB(2) levels increased significantly (p < 0.05) in both hemisphere and brainstem 5 min posttrauma. Fifteen minutes after injury, both PGE(2) and TxB(2) levels remained elevated but the levels were lower than at 5 min in the rats that did not exhibit posttraumatic seizures. This decrease in PG levels at 15 min was not observed in the rats that had seizures after injury and both PGE(2) and TxB(2) levels remained high in hemispheres and brainstem. Thus, fluid percussion brain injury results in substantial elevations in PGE(2) and TxB(2) levels and posttraumatic seizures exacerbate the observed increases.