Shapira Y, Davidson E, Weidenfeld Y, Cotev S, Shohami E
Department of Anesthesiology, Hebrew University Hadassah Medical School, Jerusalem, Israel.
J Cereb Blood Flow Metab. 1988 Jun;8(3):395-402. doi: 10.1038/jcbfm.1988.75.
Head trauma was induced in rats by a weight-drop device, falling over the exposed skull over the left hemisphere. The neurological state of the rats was evaluated by a neurological severity score at 1 h and 18 h post head trauma. At 18 h post head trauma, rats were decapitated and tissue from the vicinity of the injury and from a corresponding area in the contralateral hemisphere was taken for specific gravity (SG) determination using linear gradient columns. Slices were taken from the same sites for incubation in Krebs-Ringer solution, and the concentrations of prostaglandin (PG)E2, 6-keto-PGF1 alpha, and thromboxane B2 accumulated in the medium during 1 h were measured by radioimmunoassay. In one experimental group, rats were pretreated with intraperitoneal dexamethasone sodium phosphate (4 mg/kg) 18 and 2 h before head trauma, and a third dose was given 8 h post head trauma. Another group was treated with intraperitoneal indomethacin (10 mg/kg) 1 h before and 7 h after head trauma. Other groups were treated immediately and 8 h after head trauma with 4, 8, 15, or 30 mg/kg of dexamethasone sodium phosphate. Another group of rats was treated with free dexamethasone (10 mg/kg) right after head trauma and 8 h later. Head trauma induced edema, as expressed by decreased SG, in the left hemisphere of all traumatized rats. Neither treatment protocol affected the neurological severity score of the injured rats or the SG of the contused hemisphere. PG synthesis, on the other hand, was significantly reduced following indomethacin or free dexamethasone, both in sham and traumatized rats, but not in dexamethasone sodium phosphate-treated rats. We conclude that pretreatment with indomethacin, dexamethasone sodium phosphate, or dexamethasone, used in the present protocols, does not affect posttraumatic cerebral edema. Thus, the role of PGs as mediators of edema formation remains unclear.
通过重物下落装置对大鼠造成头部创伤，重物落在左半球暴露的颅骨上。在头部创伤后1小时和18小时，通过神经严重程度评分评估大鼠的神经状态。在头部创伤后18小时，将大鼠断头，取损伤附近组织和对侧半球相应区域的组织，使用线性梯度柱测定比重（SG）。从相同部位取材制成切片，置于Krebs-Ringer溶液中孵育，通过放射免疫分析法测定孵育1小时期间培养基中积累的前列腺素（PG）E2、6-酮-PGF1α和血栓素B2的浓度。在一个实验组中，大鼠在头部创伤前18小时和2小时腹腔注射磷酸地塞米松钠（4mg/kg），并在头部创伤后8小时给予第三剂。另一组在头部创伤前1小时和创伤后7小时腹腔注射吲哚美辛（10mg/kg）。其他组在头部创伤后立即和8小时分别给予4、8、15或30mg/kg的磷酸地塞米松钠。另一组大鼠在头部创伤后立即和8小时后给予游离地塞米松（10mg/kg）。所有受创伤大鼠的左半球均因头部创伤出现水肿，表现为SG降低。两种治疗方案均未影响受伤大鼠的神经严重程度评分或挫伤半球的SG。另一方面，在假手术组和受创伤大鼠中，吲哚美辛或游离地塞米松治疗后PG合成均显著降低，但磷酸地塞米松钠治疗的大鼠未出现此现象。我们得出结论，本实验方案中使用的吲哚美辛、磷酸地塞米松钠或地塞米松预处理不影响创伤后脑水肿。因此，PG作为水肿形成介质的作用仍不清楚。
