Esen Figen, Erdem Tulin, Aktan Damla, Kalayci Rivaze, Cakar Nahit, Kaya Mehmet, Telci Lutfi
Department of Anesthesiology and Intensive Care, University of Istanbul, Istanbul Faculty of Medicine, Istanbul, Turkey.
J Neurosurg Anesthesiol. 2003 Apr;15(2):119-25. doi: 10.1097/00008506-200304000-00009.
In this study, we examined the effects of magnesium sulfate administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats. Seventy-one adult male Sprague-Dawley rats were anesthetized, and experimental closed head trauma was induced by allowing a 450-g weight to fall from a 2-m height onto a metallic disk fixed to the intact skull. Sixty-eight surviving rats were randomly assigned to receive an intraperitoneal bolus of either 750 micromol/kg magnesium sulfate (group 4; n = 30) or 1 mL of saline (group 2; n = 30) 30 minutes after induction of traumatic brain injury; 39 nontraumatized animals received saline (group 1; n = 21) or magnesium sulfate (group 3; n = 18) with an identical protocol of administration. Brain water content and brain tissue specific gravity, as indicators of brain edema, were measured 24 hours after traumatic brain injury. Blood-brain barrier integrity was evaluated quantitatively 24 hours after injury by spectrophotometric assay of Evans blue dye extravasations. In the magnesium-treated injured group, brain water content was significantly reduced (left hemisphere: group 2, 83.2 +/- 0.8; group 4, 78.4 +/- 0.7 [P <.05]; right hemisphere: group 2, 83.1 +/- 0.7; group 4, 78.4 +/- 0.5. [P <.05]) and brain tissue specific gravity was significantly increased (left hemisphere: group 2, 1.0391 +/- 0.0008; group 4, 1.0437 +/- 0.001 [P <.05]; right hemisphere, group 2, 1.0384 +/- 0.001; group 4, 1.0442 +/- 0.005 [P <.05]) compared with the saline-treated injured group. Evans blue dye content in the brain tissue was significantly decreased in the magnesium-treated injured group (left hemisphere: group 2, 0.0204 +/- 0.03; group 4, 0.0013 +/- 0.0002 [P <.05]; right hemisphere: group 2, 0.0064 +/- 0.0009; group 4, 0.0013 +/- 0.0003 [P <.05]) compared with the saline-treated injured group. The findings of the present study support that beneficial effects of magnesium sulfate exist after severe traumatic brain injury in rats. These results also indicate that a blood-brain barrier permeability defect occurs after this model of diffuse traumatic brain injury, and magnesium seems to attenuate this defect.
在本研究中，我们检测了硫酸镁给药对大鼠实验性创伤性脑损伤后脑水肿和血脑屏障破坏的影响。71只成年雄性Sprague-Dawley大鼠接受麻醉，通过让一个450克的重物从2米高度落到固定在完整颅骨上的金属盘上，诱导实验性闭合性颅脑外伤。68只存活的大鼠在创伤性脑损伤诱导后30分钟被随机分配接受腹腔注射750微摩尔/千克硫酸镁（第4组；n = 30）或1毫升生理盐水（第2组；n = 30）；39只未受伤的动物按照相同的给药方案接受生理盐水（第1组；n = 21）或硫酸镁（第3组；n = 18）。在创伤性脑损伤后24小时测量脑含水量和脑组织比重，作为脑水肿的指标。在损伤后24小时通过分光光度法测定伊文思蓝染料外渗来定量评估血脑屏障的完整性。在镁治疗的损伤组中，与生理盐水治疗的损伤组相比，脑含水量显著降低（左半球：第2组，83.2±0.8；第4组，78.4±0.7 [P <.05]；右半球：第2组，83.1±0.7；第4组，78.4±0.5 [P <.05]），脑组织比重显著增加（左半球：第2组，1.0391±0.0008；第4组，1.0437±0.001 [P <.05]；右半球，第2组，1.0384±0.001；第4组，1.0442±0.005 [P <.05]）。与生理盐水治疗的损伤组相比，镁治疗的损伤组脑组织中的伊文思蓝染料含量显著降低（左半球：第2组，0.0204±0.03；第4组，0.0013±0.0002 [P <.05]；右半球：第2组，0.0064±0.0009；第4组，0.0013±0.0003 [P <.05]）。本研究结果支持硫酸镁在大鼠重度创伤性脑损伤后存在有益作用。这些结果还表明，在这种弥漫性创伤性脑损伤模型后会出现血脑屏障通透性缺陷，而镁似乎能减轻这种缺陷。
