参附注射液治疗重型颅脑损伤临床分析

目的探讨参附注射液应用于重型颅脑损伤患者的脑保护作用。方法将50例重型颅脑损伤患者随机分成参附治疗组24例及对照组26例。对照组予以脱水、激素、止血、抗感染等常规治疗,参附治疗组在常规治疗基础上,在伤后早期给予参附注射液3 ml/kg,分3次,连续使用10 d。所有患者行颅内压监测。观察两组患者的最高颅内压、觉醒天数,甘露醇使用天数及剂量,并发症并对预后评估。结果参附治疗组颅内压控制更为良好,觉醒时间缩短,并发症降低,预后明显改善。结论参附注射液对重型颅脑损伤具有一定的脑保护作用。     

氯胺酮对脑外伤大鼠脑组织水通道蛋白-4表达的影响

目的 观察氯胺酮对脑外伤大鼠脑组织水通道蛋白-4（AQP-4）表达的影响，探讨氯胺酮减轻脑外伤的作用机制。方法 健康雄性Wistar大鼠152只，随机分为对照组和治疗组，每组76只。采用自由落体致脑外伤动物模型，治疗组大鼠伤后1 h腹腔注射氯胺酮120 mg／kg，对照组相同时间给予容量生理盐水。每组分别在伤后6、12、24、48和72h随机处死15只大鼠，每个时点的5只大鼠用于测定脑组织含水量，每个时点的其余10只大鼠经心脏灌注后取脑组织，观察脑组织病理学改变及神经元凋亡情况，测定AQP-4表达。结果 与对照组比较，治疗组大鼠伤后各时间点脑含水量、AQP-4表达及神经元凋亡计数均降低（P〈0．05或0．01），脑组织病理学改变明显减轻。结论 氯胺酮120 mg／kg通过抑制脑外伤大鼠脑组织AQP-4的表达，减少了神经元的凋亡，从而减轻脑损伤。     

异丙酚对脑创伤家兔血/脑脊液乳酸和葡萄糖含量的影响

目的探讨异丙酚对家兔脑创伤的影响.方法用90只健康新西兰兔(雄性)建立稳定的脑创伤模型.1.将20只家兔随机分为对照组噻胺酮1mg/kg(n=10)与异丙酚(Pro)组噻胺酮1mg/kg+异丙酚30mg@kg-1@h-1.麻醉动物,维持30min(n=10).分别于伤前、伤后4h、24h、48h、72h、1w采集外周静静脉血与脑脊液,测定血/脑脊液乳酸(LA)和葡萄糖(Glu)含量;2.将70只家兔随机分为对照组,伤后24h组、72h组和1w组(输注生理盐水)以及伤后异丙酚治疗24h组、72h组和1w组(异丙酚30mg@kg-1@h-1.静脉滴注,每次维持30min,每天一次)(n=10),分别取脑组织做NSE免疫组织化学染色和病理检查.结果1.两组伤后血/脑脊液LA水平显著高于伤前(P＜0.01),但异丙酚组明显低于同时段对照组水平(P＜0.05或0.01);对照组伤后24h、48h和72h血/脑脊液Glu明显低于伤前,异丙酚组脑脊液Glu仅在伤后24h降低(P＜0.05或0.01),异丙酚组血Glu在伤后4h、24h与对照组比较有明显差异(P＜0.05).2.脑组织NSE免疫组织化学染色和病理检查对照组损伤区及其周围脑组织伤后24h起可见脑组织出血,退行性变,胶质细胞减少,部分区域细胞可见空泡变性;伤后72h可见较多嗜中性细胞浸润;伤后1w脑间质水肿,胶质细胞明显增生,神经元细胞未见NSE表达.异丙酚组在受伤脑组织或其周围损伤明显轻于对照组,部分神经元细胞NSE表达明显.结论异丙酚能够降低脑创伤后血/脑脊液LA含量,对创伤性脑损伤具有一定的保护作用.     

乌司他丁对急性重型颅脑损伤患者颈静脉球部血清UCH-L1、CK-BB的影响研究

目的探讨乌司他丁对72例急性重型颅脑损伤患者颈静脉球部血清UCH-L1、CKBB的影响。方法对符合受试条件的急性重型颅脑损伤患者入院后采用随机数字表法分为两组:治疗组36例和对照组36例。治疗组给予静脉注射乌司他丁20万U每8小时1次;对照组给予静脉注射生理盐水20ml每8小时1次。采用双抗体夹心酶标免疫法检测72例急性重型颅脑损伤患者在伤后12小时、24小时、第48小时、第3天、第5天、第7天的颈静脉球部血清泛素羧基末端水解酶L1(Ubiquitin carboxy terminal hydrolases L1,UCH-L1)、脑型肌酸激酶同工酶(Creatine kinase brain band isoenzyme,CK-BB)的变化,探讨乌司他丁对急性重型颅脑损伤患者的脑保护效果和可能机制。结果治疗组在急性重型颅脑损伤患者伤后12小时、24小时、第48小时、第3天、第5天、第7天颈静脉球部血清UCH-L1、CK-BB浓度均低于对照组(F=15.33,P0.01;F=36,P0.01)。结论使用乌司他丁可以降低急性重型颅脑损伤患者颈静脉球部血清UCH-L1、CKBB水平,在伤后早期有神经保护作用,促进患者神经功能恢复。     

高压氧对重型颅脑损伤的疗效研究

目的观察高压氧对重型颅脑损伤的治疗效果,并分析其作用机制。方法 80例重型颅脑损伤患者随机分为高压氧治疗组(n=40)和对照组(n=40),观察两组患者的清醒人数,清醒时间,GCS评分的变化,治疗3个月的GOS评分、病死和植物状态比例,并分析两组的临床疗效,同时监测治疗前后脑动脉血流速度变化。结果治疗组的清醒人数的比例明显高于对照组(P0.05),觉醒平均时间较对照明显缩短(P0.05),3疗程后GCS评分和3个月后的GOS评分明显高于对照组(P0.05),植物状态及死亡率较对照组低(P0.05),治愈率及总有效率明显高于对照组(P0.01);治疗组2个疗程血流速度较对照组下降明显(P0.05)。结论早期行高压氧治疗对重型颅脑损伤具有明显疗效,可能与高压氧能有效提高血氧含量、扩大血氧弥散半径、促进血管生成和侧枝循环建立、有效缓解脑血管痉挛状态、清除自由基、减少缺血区脑细胞凋亡等作用有关。     

镁离子制剂治疗重型颅脑损伤的临床研究

目的探讨镁离子制剂治疗重型颅脑损伤的疗效和安全性.方法选择GCS评分5～8分患者60例,采用随机双盲前瞻性临床对照研究方法分组,治疗组在综合常规治疗基础上,在伤后24小时内静滴硫酸镁针,每日应用硫酸镁针20ml,连续治疗10天,对照组给予一般综合常规治疗.分析对比治疗前后和治疗过程中患者的病情和重要辅助检查指标的变化趋势,并同时对比随访结束时患者神经功能恢复情况和生活质量状况,并对结果进行统计学分析.结果治疗组GCS评分在用药后第5天开始明显优于对照组(P＜0.05),治疗结束后和随访结束后治疗组GOS评分明显优于对照组(P＜0.05),治疗组伤残情况、并发症等也明显优于对照组(火0.05).试验过程中未发现用药造成的毒副反应.结论早期及时补充镁离子能促进重型颅脑损伤患者神经功能恢复,降低致残率,改善远期生活质量,并具有相当可靠的安全性.     

甲基强的松龙对脊髓爆震伤后运动神经元形态学改变的实验研究

目的观察甲基强的松龙(MP)冲击疗法在脊髓爆震伤后早期救治中的疗效.方法将48只家兔随机分为6h生理盐水组(A组)、24h生理盐水组(B组)、48h生理盐水组(C组)、6h MP组(D组)、24h MP组(E组)及48h MP组(F组),每组8只,采用0.9g黑索金(RDX)对每只家兔进行爆震,伤后1h内A、B、C组给予静脉输入生理盐水,速度为5ml/kg/h,D、E、F组根据NASCISⅡ方案给予MP,A、D组于伤后6h取材,B、E组于伤后24h取材,C、F于伤后48h取材,观察脊髓前角运动神经元的形态和数量的变化.结果爆震伤后6h脊髓运动神经元出现可逆性改变,伤后24h脊髓死亡运动神经元达到最多,并且持续到伤后48h,伤后1h内给予MP冲击治疗后,24h、48h组与对照组相比在正常与坏死神经元的数量方面均表现出显著的统计学差异(P＜0.001).结论脊髓爆震伤后早期给予MP冲击治疗,对脊髓运动神经元具有保护作用.     

不同降温方式对脑外伤后伤灶区c-fos mRNA和神经生长因子表达的影响

目的 通过对大鼠重型脑挫裂伤后体温的干预,观察不同降温方式对脑外伤后伤灶区c-fos mRNA和神经生长因子(nerve growth factor,NGF)表达的影响,了解其表达强度是否与伤后不同降温方式对脑损伤的保护机制有关. 方法 健康成年SD大鼠336只,随机分为四组(每组84只),除假手术组外各组动物均按自由落体法造成重度脑挫裂伤;每组又按处死时间分为七个亚组(每亚组12只),分别检测c-fos mRNA(6只)与NGF(6只)的表达. 结果 ①伤后4h、8h、12 h与24h,全身亚低温组与局部亚低温组c-fos mRNA表达明显高于TBI组(P＜0.01),其他各时点无差异;TBI组在伤后4h、8h、12 h、24h与3d,c-fos mRNA表达均明显高于假手术组(P＜0.01).②伤后4h、8h,全身亚低温组与局部亚低温组NGF表达与TBI组无明显差异(P＞0.05);而在伤后12 h、24h、3d、5d与7d,两亚低温组NGF表达明显高于TBI组((P＜0.05或P＜0.01).③全身亚低温组与局部亚低温组在伤后各时间点c-fos mRNA和NGF表达无显著性差异(P＞0.05). 结论 脑外伤后亚低温可促进c-fos mRNA和NGF表达上调,全身亚低温与局部亚低温两种不同降温方式无明显差异.     

牛磺酸对严重烧伤大鼠心肌损害的保护作用

目的　观察牛磺酸(Tau)对严重烧伤大鼠心肌损害的作用。　方法　将Wistar大鼠随机分为对照组(10只,不致伤)、烧伤组(60只)和Tau治疗组(60只)。后两组大鼠造成30%TBSAⅢ度烫伤(以下称烧伤),烧伤组伤后常规补液,Tau治疗组伤后腹腔注射Tau400mg/kg.于两组烧伤大鼠伤后1、3、6、12、24、48h检测其血浆中心肌肌钙蛋白T(cTnT)、丙二醛(MDA)的含量以及血浆、心肌组织中肿瘤坏死因子α(TNF- α)、血管紧张素Ⅱ(AngⅡ)的含量、心肌钙离子水平,用透射电镜观察心肌组织形态结构变化,并与对照组的上述指标进行比较。将烧伤组大鼠血浆TNF- α、AngⅡ检测结果分别与cTnT检测结果作相关性分析。　结果　烧伤组大鼠伤后3h起血浆cTnT水平较对照组(0.16±0. 03)μg/L显著升高(P<0. 01), 12h达峰值(6. 32±0. 41)μg/L, 48h仍显著高于对照组(P<0. 01).烧伤组伤后3—48h血浆MDA含量及心肌钙离子水平明显高于对照组(P<0. 01 );伤后6—48h血浆和心肌组织TNF- α含量显著高于对照组(P<0. 01);血浆及心肌组织中AngⅡ水平分别于伤后1—24h、3—24h明显高于对照组(P<0. 01).Tau治疗组上述指标在伤后多数时相点明显低于烧伤组(P<0. 01). 烧伤组大鼠伤后早期心肌肌丝断裂溶解、线粒体肿胀、嵴减少,Tau治疗组心肌组织接近正常。烧伤组     

甲基强的松龙对大鼠颅脑损伤后细胞间黏附分子-1的影响

目的　观察甲基强的松龙对大鼠颅脑损伤后脑组织中细胞间黏附分子 (ICAM ) 1含量的影响 ,探讨其作用机制。方法　将 5 5只SD大鼠随机分为 3组 ,采用骨窗形成后硬膜外打击法造成鼠脑挫裂伤模型 ,正常组 5只 ,麻醉后 ,只行开颅手术 ,不作头颅打击 ;治疗组致伤后腹腔内注射 3 0mg/kg体重甲基强的松龙 ,对照组腹腔内注射 3 0mg/kg体重生理盐水。对照组和治疗组分别在伤后 6、2 4、48、72、96h断头取脑 ,对脑组织中ICAM 1含量进行检测。结果　治疗组脑皮质中的ICAM 1活性在伤后 6h较对照组升高 (P <0 .0 1) ,48h达高峰后开始下降 ,96h降至基础水平。甲基强的松龙治疗组在伤后 6～ 48hICAM 1活性较对照组明显降低 (P <0 .0 5 )。结论　颅脑损伤后 ,受损脑组织中ICAM 1含量升高 ,甲基强的松龙可通过抑制损伤后ICAM 1活性 ,起到保护创伤神经元的作用。     

硫酸镁对急性重型颅脑损伤患者血清S-100B蛋白浓度的影响

目的通过动态观察硫酸镁对急性重型颅脑损伤患者血清S-100B蛋白浓度的影响，进一步探讨硫酸镁在急性重型颅脑损伤治疗中的作用。方法将120例急性重型颅脑损伤患者随机分为硫酸镁组和常规组。硫酸镁组在常规治疗的基础上，予25％硫酸镁8ml用生理盐水稀释至100ml匀速静脉推注，时间为15分钟。然后将25％硫酸镁30ml加入5％葡萄糖500ml中用24小时缓慢静脉滴注，输液泵控制输液速度，连续用7天。所有患者于入院6小时内，入院后第2、3、4、5、6天动态检测血清S-100B蛋白浓度。3个月后对患者进行GOS评估。结果硫酸镁组和常规组血清S-100B蛋白浓度明显高于正常对照组（P〈0，05）；硫酸镁组血清S-100B蛋白浓度明显低于常规组（P〈0．05）；硫酸镁能够改善急性熏型颅脑损伤患者的预后。结论急性重型颅脑损伤患者血清S-100B蛋白浓度明显升高，早期应用硫酸镁能显著降低患者血清S-100B蛋白浓度，保护神经功能．改善预后。     

Effects of magnesium sulfate on traumatic brain edema in rats

svarietyofneuroprotectiveagentshavebeensynthesized .However ,besidessomeagentspresentlybeingevaluatedinclinicaltrails ,mostofthesecompoundshavelimitedclinicalusebecauseofneurotoxicityandbehavioralsideeffects .Recently ,severalstudiesdemonstratedthattraumaticinjurytothebraincausesadecreaseinmagnesiumconcentrationcorrelatedwithinjuryseverity .1Sincethen ,moreandmoreattentionhasbeen paidtoMgSO4 foritsneuroprotectiveeffects .Magnesiumsulfatehasbeenwidelyusedinclinicalpracticeforalmost 10 0 years.…     

Effects of magnesium sulfate on traumatic brain edema in ats

OBJECTIVE: To investigate the effects of magnesium sulfate on traumatic brain edema and explore its possible mechanism. METHODS: Forty-eight Sprague-Dawley (SD) rats were randomly divided into three groups: Control, Trauma and Treatment groups. In Treatment group, magnesium sulfate was intraperitoneally administered immediately after the induction of brain trauma. At 24 h after trauma, total tissue water content and Na(+), K(+), Ca(2+), Mg(2+) contents were measured. Permeability of blood-brain barrier (BBB) was assessed quantitatively by Evans Blue (EB) dye technique. The pathological changes were also studied. RESULTS: Water, Na(+), Ca(2+) and EB contents in Treatment group were significantly lower than those in Trauma group (P<0.05). Results of light microscopy and electron microscopy confirmed that magnesium sulfate can attenuate traumatic brain injury and relieve BBB injury. CONCLUSIONS: Treatment with MgSO4 in the early stage can attenuate traumatic brain edema and prevent BBB injury.     

丙泊酚对脑创伤家兔血清和脑脊液肌酸激酶、乳酸脱氢酶活性的影响

目的：观察丙泊酚麻醉对脑创伤家兔血清（s)，脑脊液（csf)肌酸激酶（CK），乳酸脱氢酶（LDH）的指标变化，探讨丙泊酚对家兔脑创伤的影响及其意义。方法：取20只健康新西兰兔建立稳定的脑创伤模型，随机分为对照组（C组）和丙泊酚组（P组），分别于伤前，伤后4，24，48，72小时和伤后7天测定血清及脑脊液CK，LDH活性。结果：C组s-CK和csf-CK,s-LDH和csf-LDH显著高于伤前（P＜0．01）,P组伤后48。72小时，7天s-CK和csf-CK显著低于C组（P＜0．01），s-LDH在伤后72小时显著低于C组（P＜0．01）,csf-LDH在伤后48小时，7天明显低于C组（P＜0．05），结论：脑创伤后，s-CK和csf-CK,s-LDH和csf-LDH活性均明显增高，丙泊酚能显著降低血及脑脊液CK、LDH活性，提示丙泊酚能够改善脑代谢，对创伤性脑损伤具有一定的脑保护作用。     

Magnesium sulfate treatment in experimental spinal cord injury: emphasis on vascular changes and early clinical results

Injury to the spinal cord results in disruption of neurons, cell membranes, axons, myelin, and endothelial cells. The aim of this study was to demonstrate the protective effect of magnesium sulfate on the blood-spinal cord barrier after acute spinal cord injury (SCI). This experiment was conducted in two parts. In the first, rats were injected intravenously with Evans blue 2 h after SCI. The laminectomy-only group had no trauma. Contusion injury (50 g-cm) was applied to the trauma and treatment groups. Magnesium sulfate (600 mg/kg) was given to the treatment group immediately after injury. For the second part, clinical evaluations were performed 24 h post surgery. Then, following Evans blue injection, spinal cord samples were obtained from the laminectomy-only, trauma, and treatment groups. For the control group, nontraumatized spinal cord samples were taken after Evans blue injection following clinical examination. Laminectomy did not affect the spinal cord Evans blue content in 2-h and 24-h groups. The trauma increased tissue Evans blue content, and 24-h samples showed more remarkable tissue Evans blue content, suggesting secondary injury. Application of 600 mg/kg of magnesium resulted in lower Evans blue content in the spinal cord than with injury. Remarkable clinical neuroprotection was observed in the treatment groups. Magnesium sulfate showed vaso- and neuroprotective properties after contusion injury to the rat spinal cord. The authors also demonstrated secondary injury of the blood-spinal cord barrier with the Evans blue clearance technique for the first time.     

Effects of nimodipine and magnesium sulfate on endogenous antioxidant levels in brain tissue after experimental head trauma.

To examine the effects of calcium antagonists nimodipine and magnesium sulfate (MgSO4) on tissue endogenous antioxidant levels, the authors studied superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels in rabbit brain 1 hour after experimental head trauma. Forty New Zealand rabbits were anesthetized and randomly divided into four groups. Group 1 (n = 10) was the sham operated group. Group 2 (n = 10), the control group, received head trauma and no treatment. Group 3 (n = 10) received head trauma and intravenous (IV) 2 microgr/kg nimodipine. Group 4 (n = 10) received head trauma and IV 100 mg/kg MgSO4. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 20 g from a height of 40 cm. In the right (traumatized) hemisphere, SOD and GPx decreased by 57.60% +/- 9.60% and 72.93% +/- 5.51% respectively from sham values. Magnesium sulfate, but not nimodipine, reduced the magnitude of decrease of SOD and GPx to 19.43% +/- 7.15% and 39.01% +/- 7.92% respectively from sham values. In the left (nontraumatized) hemisphere, MgSO4 increased SOD to 42.43% +/- 24.76% above sham values. The authors conclude that MgSO4 treatment inhibited the decrease in SOD and GPx levels in experimental brain injury.     

Magnesium deficiency exacerbates and pretreatment improves outcome following traumatic brain injury in rats: 31P magnetic resonance spectroscopy and behavioral studies

The biochemical mechanisms mediating delayed or secondary tissue injury after central nervous system trauma remain speculative. We have demonstrated previously that traumatic brain injury in rats causes a rapid decline in tissue intracellular free magnesium [Mg]f and total magnesium [Mg]t concentrations, which were significantly correlated with injury severity. In order to examine the relationship between magnesium and traumatic brain injury, we assessed whether (1) magnesium deficiency exacerbates or (2) magnesium treatment improves posttraumatic outcome following fluid-percussion brain injury (2.0-2.4 atm) in rats. Animals placed on magnesium-deficient diet for 14 days showed a 15% decrease in brain [Mg]f as measured by phosphorus (31P) magnetic resonance spectroscopy (MRS). Magnesium deficiency significantly exacerbated neurologic dysfunction and increased mortality following injury when compared to normally fed saline-treated controls. Conversely, pretreatment with magnesium sulfate (0.1 mEq) 15 min before brain injury prevented the fall in [Mg]f observed by 31P MRS in saline-treated animals and significantly improved both cellular bioenergetic state and chronic posttraumatic neurologic outcome. These combined observations suggest that alterations in brain [Mg]f after trauma may play a role in the pathophysiology of traumatic brain injury.     

硫酸镁对弥漫性脑损伤脑组织的保护作用及机制

目的 探讨硫酸镁对于弥漫性脑损伤脑组织可能的保护机制.方法 依据Marmarou's弥漫性脑损伤动物模型有改进,采用成年健康SD雄性大鼠,体质量325～375 g,共50只.其中,外伤组25只,干预组25只(两组外伤后12、24、48、72 h,1周,每组各5只).干预组应用微泵给予硫酸镁静脉注射治疗,外伤后大鼠自由进食水,按时间段处死大鼠,提取大鼠皮层脑组织,应用实时逆转录.聚合酶链反应(realtime RT-PCR)检测外伤组与干预组不同时间段ET-1 mRNA、iNOS mRNA表达,另取脑组织应用脑组织干湿重比表示脑组织含水量.结果 ET-1 mRNA表达干预组较外伤组干预组降低,应用成组t检验分析方法检验可得:6、12、24、48 h组组间差异有统计学意义(P<0.01),72 h,1周组间比较差异无统计学意(P>0.05).iNOS mRNA表达干预组较外伤组降低,干预组与外伤组相应时间组组间差异有统计学意义(P<0.01).结论 应用微泵静脉注射硫酸镁早期减少了ET-1 mRNA、iNOS mRNA的表达,从而使ET-1、iNOS、NO合成减少,减轻了脑组织缺血缺氧及对脑细胞的毒性,从而使干预组弥漫性脑损伤大鼠脑组织含水量较单纯外伤组弥漫性脑损伤大鼠脑组织含水量减少的原因.     

Effects of magnesium sulfate on brain mitochondrial respiratory function in rats after experimental traumatic brain injury

Objective:To study the effects of magnesium sulfate on brain mitochondrial respiratory function in rats after experimental traumatic brain injury and the possible mechanism.Methods:The middle degree brain injury in rats was made by BIM-III multi-function impacting machine.The brain mitochondrial respiratory function was measured with oxygen electrode and the ultra-structural changes were observed with transmission electron microscope(TEM).Results:1.The brain mitochondrial respiratory stage III and respiration control rate reduced significantly in the untreated groups within 24 and 72 hours.But treated Group A showed certain degree of recovery of respiratiory function;treated Group B showed further improvement.2. Untreated Group,treated Groups A and B had different degrees of mitochondrial ultra-structural damage respectively, which could be attenuated after the treatment with magnesium sulfate.Conclusions:The mitochondrial respiratory function decreases significantly after traumatic brain injury.But it can be apparently improved after magnesium sulfate management along with the attenuated damage of mitochondria discovered by TEM.The longer course of treatment can obtain a better improvement of mitochondrial respiratory function.     

Effects of magnesium administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats

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.