Feldman Z, Gurevitch B, Artru A A, Oppenheim A, Shohami E, Reichenthal E, Shapira Y
Department of Neurosurgery, Soroka Medical Center, Ben-Gurion University, Beer-Sheva, Israel.
J Neurosurg. 1996 Jul;85(1):131-7. doi: 10.3171/jns.1996.85.1.0131.
Excitatory amino acids (EAA), mainly glutamate and aspartate, are released in excessive amounts from terminals of ischemic or traumatically injured neurons. These excessive levels of EAAs initiate a cascade of events believed to lead to secondary delayed damage to the surrounding brain. The N-methyl-D-aspartate receptor antagonists MK-801 and ketamine are reported to suppress excessive EAA release and to attenuate the development of focal brain edema following neuronal injury. Magnesium is also reported to work at the postsynaptic receptor to reduce the neurotoxic effect of glutamate. The present study was undertaken to examine the effect of postinjury treatment with Mg++ on brain edema and neurological outcome after traumatic brain injury. Sixty-nine rats that survived halothane anesthesia and closed head trauma (CHT) were randomly assigned to one of seven experimental groups: sham, CHT, and CHT with administration of Mg++ 1 hour postinjury. At 48 hours, brain tissue Mg++ concentration (calculated from optical density using a standard curve) was significantly increased compared to baseline levels (10.06 +/- 2.44 mg/g vs. 6.83 +/- 0.81 mg/g, p < 0.01 calculated by one-way analysis of variance). Also at 48 hours postinjury, brain tissue specific gravity in the contused hemisphere of Mg(++)-treated rats was significantly greater than that in the contused hemisphere of untreated rats, indicating attenuation of brain edema formation by Mg++. The neurological severity score (NSS) of rats treated with Mg++ improved significantly at both 18 and 48 hours, compared to baseline values obtained 1 hour after CHT but prior to administration of Mg++ (11.2 +/- 2.5 vs. 15.2 +/- 4.1, p = 0.03; and 12.3 +/- 6.1 vs. 17.3 +/- 3.6, p = 0.004, respectively). In the untreated groups, the NSS at 18 and 48 hours was not significantly different from baseline values (that is, no neurological improvement). The present study indicates that postinjury treatment with Mg++ attenuates brain edema formation and improves neurological outcome after experimental CHT.
兴奋性氨基酸（EAA），主要是谷氨酸和天冬氨酸，在缺血或受创伤的神经元终末中大量释放。这些过高水平的EAA引发一系列事件，据信会导致对周围脑组织的继发性延迟损伤。据报道，N-甲基-D-天冬氨酸受体拮抗剂MK-801和氯胺酮可抑制EAA的过量释放，并减轻神经元损伤后局灶性脑水肿的发展。也有报道称镁作用于突触后受体，以降低谷氨酸的神经毒性作用。本研究旨在探讨损伤后用Mg++治疗对创伤性脑损伤后脑水肿和神经功能转归的影响。六十九只在氟烷麻醉和闭合性颅脑损伤（CHT）后存活的大鼠被随机分为七个实验组之一：假手术组、CHT组以及损伤后1小时给予Mg++的CHT组。在48小时时，与基线水平相比，脑组织Mg++浓度（使用标准曲线根据光密度计算）显著升高（10.06±2.44mg/g对6.83±0.81mg/g，单向方差分析计算得出p<0.01）。同样在损伤后48小时，Mg++处理组大鼠挫伤半球的脑组织比重显著高于未处理组大鼠挫伤半球的脑组织比重，表明Mg++减轻了脑水肿的形成。与CHT后1小时但在给予Mg++之前获得的基线值相比，Mg++处理组大鼠的神经严重程度评分（NSS）在18小时和48小时时均显著改善（分别为11.2±2.5对15.2±4.1，p=0.03；以及12.3±6.1对17.3±3.6，p=0.004）。在未处理组中，18小时和48小时时的NSS与基线值无显著差异（即无神经功能改善）。本研究表明，损伤后用Mg++治疗可减轻实验性CHT后脑水肿的形成并改善神经功能转归。
