Dewitt D S, Kong D L, Lyeth B G, Jenkins L W, Hayes R L, Wooten E D, Prough D S
Department of Anesthesia, Bowman Gray School of Medicine, Winston-Salem, North Carolina.
J Neurotrauma. 1988;5(4):303-13. doi: 10.1089/neu.1988.5.303.
Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) 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 micrograms/ml). PGE2 and TxB2 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. PGE2 and TxB2 levels increased significantly (p less than 0.05) in both hemisphere and brainstem 5 min posttrauma. Fifteen minutes after injury, both PGE2 and TxB2 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 PGE2 and TxB2 levels remained high in hemispheres and brainstem. Thus, fluid percussion brain injury results in substantial elevations in PGE2 and TxB2 levels and posttraumatic seizures exacerbate the observed increases.
在实验性创伤性脑损伤后的大鼠中测量了前列腺素E2（PGE2）和血栓素B2（TxB2）水平。将大鼠（n = 36）在戊巴比妥麻醉下制备用于液压冲击性脑损伤。24小时后，使用甲氧氟烷对大鼠进行轻度麻醉，致伤（2.3大气压），并在5或15分钟后处死。12只大鼠在伤前死亡，未纳入分析。以下组用于数据分析：I组（n = 6）为准备致伤但未致伤的假伤大鼠；II组（n = 6）致伤并在5分钟后处死；III组（n = 12）致伤并在创伤后15分钟处死。在通过断头法将所有大鼠放入液氮中处死前30秒，静脉注射消炎痛（3mg/kg）以防止死后PG合成。处死大鼠后，取出大脑，称重，并在含有消炎痛（50μg/ml）的少量磷酸盐缓冲液中匀浆。使用双标记放射免疫测定法测定PGE2和TxB2水平。在III组的12只大鼠中有5只观察到创伤后惊厥，这些大鼠单独进行分析。创伤后5分钟，大脑半球和脑干中的PGE2和TxB2水平均显著升高（p < 0.05）。损伤后15分钟，PGE2和TxB2水平仍升高，但在未出现创伤后惊厥的大鼠中，其水平低于5分钟时。在损伤后出现惊厥的大鼠中未观察到15分钟时PG水平的这种下降，大脑半球和脑干中的PGE2和TxB2水平仍保持较高。因此，液压冲击性脑损伤导致PGE2和TxB2水平大幅升高，创伤后惊厥加剧了观察到的升高。
