Effect of Xingnaojing injection on cerebral edema and blood-brain barrier in rats following traumatic brain injury

Objective:To explore the effects of Xingnaojing injection on cerebral edema and blood-brain barrier (BBB) in rats following traumatic brain injury (TBI).Methods: A total of 108 adult male Sprague-Dawley rats were used as subjects and randomly assigned to three groups:sham-operation,TBI and Xingnaojing injection was set up by the improved device of Feeney's weightcontent and BBB permeability expressed as Evans blue content were measured at 1, 3, 5 and 7 days after surgery.Results: In sham-operation group, brain water content and Evans blue content in brain tissue were 78.97%±1.22%and 5.13μg±0.71μg. Following TBI, water content in brain tissue was increased significantly at 1, 3, 5 and 7 days (83.49%±0.54%, 82.74%±0.72%, 80.22%±0.68%, 79.21%±0.60%), being significantly higher than that in sham operation group (P<0.05). Evans blue content was increased in TBI group (16.54 μg±0.60 μg, 14.92μg±0.71μg, 12.44 μg ±0.92μg, 10.14μg±0.52 μg) as compared with sham-operation group(P<0.05). After treatment with Xingnaojing injection, brain water content decreased as compared with TBI group (81.91%±1.04%, 80.38%±0.72%, 79.54%±0.58%,78.60%±0.77%, P<0.05). Xingnaojing injection also reduced the leakage of BBB as compared with TBI group (15.11 μg± 0.63 μg, 13.62 μg±0.85μg, 10.06 μg±0.67 μg, 9.54 μg±0.41 μg,P<0.05).Conclusion: Xingnaojing injection could alleviate cerebral edema following TBI via reducing permeability ofBBB.     

Effect of Xingnaojing injection on cerebral edema and blood-brain barrier in rats following traumatic brain injury

Objective:To explore the effects of Xingnaojing injection on cerebral edema and blood-brain barrier (BBB) in rats following traumatic brain injury (TBI).Methods: A total of 108 adult male Sprague-Dawley rats were used as subjects and randomly assigned to three groups:sham-operation,TBI and Xingnaojing injection was set up by the improved device of Feeney's weightcontent and BBB permeability expressed as Evans blue content were measured at 1, 3, 5 and 7 days after surgery.Results: In sham-operation group, brain water content and Evans blue content in brain tissue were 78.97%±1.22%and 5.13μg±0.71μg. Following TBI, water content in brain tissue was increased significantly at 1, 3, 5 and 7 days (83.49%±0.54%, 82.74%±0.72%, 80.22%±0.68%, 79.21%±0.60%), being significantly higher than that in sham operation group (P<0.05). Evans blue content was increased in TBI group (16.54 μg±0.60 μg, 14.92μg±0.71μg, 12.44 μg ±0.92μg, 10.14μg±0.52 μg) as compared with sham-operation group(P<0.05). After treatment with Xingnaojing injection, brain water content decreased as compared with TBI group (81.91%±1.04%, 80.38%±0.72%, 79.54%±0.58%,78.60%±0.77%, P<0.05). Xingnaojing injection also reduced the leakage of BBB as compared with TBI group (15.11 μg± 0.63 μg, 13.62 μg±0.85μg, 10.06 μg±0.67 μg, 9.54 μg±0.41 μg,P<0.05).Conclusion: Xingnaojing injection could alleviate cerebral edema following TBI via reducing permeability ofBBB.     

地西泮对放射性脑损伤大鼠血脑屏障的影响

目的研究照射前给予地西泮对放射性脑损伤大鼠血脑屏障的影响,探讨其对放射性脑损伤的防护作用机理。方法 240只SD大鼠随机分为4组,每组60只,D-R组:照射前30 min腹腔注射地西泮5 mg／kg;N-R组:照射前未用药;D-SR组:假照射(放置于照射野之外)前30 min腹腔注射地西泮5 mg／kg;N-SR组:假照射前未用药。D-R、N-R组建立清醒状态下大鼠放射性脑损伤模型。分别于照射前即刻、照射后6 h、1 d、1周和1月时记录磁共振成像(MRI)T1加权、T2加权的信号强度及其增强率,测定脑组织中伊文思蓝(EB)含量,免疫组化法分析海马神经元血管内皮生长因子(VEGF)的表达,并观察病理形态学的改变。结果 N-R组照射后T1加权的信号强度降低,T2加权的信号强度和信号强度的增强率升高,D-R组上述MRI的改变均比N-R组降低,D-R组脑组织EB含量在照射后6 h、1周和1月时及照射后6 h VEGF表达较N-R组降低(P<0．05或0．01)。结论在照射前使用地西泮通过降低脑组织VEGF表达,降低了放射性脑损伤大鼠血脑屏障的通透性,对放射性脑损伤有一定的防护作用。     

Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.     

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 ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury

Ｉｎｒｅｃｅｎｔｙｅａｒｓ ,ｉｔｉｓｆｏｕｎｄｔｈａｔｅｘｏｇｅｎｏｕｓｇａｎｇｌｉｏｓｉｄｅＧＭ 1ｎｏｔｏｎｌｙ ｐｒｏｍｏｔｅｃｕｌｔｕｒｅｄｎｅｕｒｏｎｓｔｏｇｅｍｍａｔｅａｎｄａｘｏｎｔｏ ｇｒｏｗｉｎｖｉｔｒｏ ,ｂｕｔａｌｓｏｐａｓｓｅｓｔｈｒｏｕｇｈｂｒａｉｎ ｂｌｏｏｄｂａｒｒｉｅｒｔｏｐｒｏｔｅｃｔｃｅｌｌｕｌａｒｍｅｍｂｒａｎｅｆｕｎｃｔｉｏｎｉｎｔｈｅｅａｒｌｙｓｔａｇｅａｎｄｈａｓｓｉｇｎｉｆｉｃａｎｔｅｆｆｅｃｔｓｏｎｒｅｓｔｏｒａｔｉｏｎｏｆｔｈｅｄａｍａｇｅｄｆｕｎｃｔ…     

Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury

Traumaticbraininjury(TBI) isamongthemostseriousinjuries, frequentlycausingdeathorpermanentdisability. ItiscloselyrelatedwiththehottesttopicsabouthowtoreducetheneurologicalimpairmentwhichmayresultfromTBI.Necrosisinthedamagedregionhadbeenconventionallythoughttobetheonlydeathmodeoftheinjuredneuronsuntilrecently. Atpresent, alotofevidencehasindicatedthatapoptosismightbeanothermainmodeofcelldeathafteraheadtrauma.1 Inthisresearch, animalmodelofTBIwasmadewithadultrabbit, apoptoticcellsweredetecte…     

Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats

ＩＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ ,ＺｈｕｊｉａｎｇＨｏｓｐｉｔａｌ ,ＦｉｒｓｔＭｉｌｉｔａｒｙＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｇｕａｎｇｚｈｏｕ 5 10 2 82 ,Ｃｈｉｎａ (ＸｕＲＸａｎｄＬｕｏＣＹ)ＳｕｐｐｏｒｔｅｄｂｙＮａｔｕｒａｌＳｃｉｅｎｃｅＦｏｕｎｄａｔｉｏｎｏｆＧｕａｎｇｄｏｎｇＰｒｏｖｉｎｃｅ (ＧＤ990 416 )ａｎｄＮａｔｕｒａｌＳｃｉｅｎｃｅＦｏｕｎｄａｔｉｏｎｏｆＣｈｉｎａ(39770 76 0 )ｔｉｓｅｘｐｅｒｉｍｅｎｔａｌｌｙｆｏｕｎｄｔｈａｔｇｌｕｔａｍａｔｅｍａｙｉｎ…     

急性高容血液稀释对犬血脑屏障受损后颅内压和脑组织含水率的影响

目的 研究在血脑屏障(BBB)开放后极端条件下急性高容血液稀释(AHH)对颅内压(ICP)和脑组织含水率的影响。方法 健康杂种犬29只,气管插管机械通气。随机分成四组;A组(对照组,n=2):机械通气60min后处死;B组(BBB完整AHH组,n=10):6％羟乙基淀粉50ml/kg,AHH 60min后处死;C组(BBB开放AHH组,n=10):麻醉后开放BBB,AHH 60min后处死;D组(BBB开放组,n=7):不行AHH,开放BBB 60min后处死。比较CVP、MAP、HR、ECG、ICP和脑组织含水率指标并在光镜下检查脑组织和细胞形态学。结果 B、C组Hct值范围分别由(37±3)％、(36.9±3.7)％降到(19.8±2.8)％、(22.9±2.1)％。A、B组ICP未见明显变化。C、D组AHH后ICP分别由(9.8±2.9)、(10.5±2.0)mmHg降为(8.2±1.7)、(6.5±1.7)mmHg。脑组织含水率四组极为接近,A～D组AHH和BBB是否开放对其未见明显影响。光镜下的形态学分析显示,A、B组无明显细胞变性,C组神经元细胞轻度水肿变性,D组神经元细胞变性较重伴轻度水肿。结论 应用6％羟乙基淀粉AHH对ICP没有显著影响,即使在BBB完全开放的情况下。当BBB开放后,AHH可致神经元和胶质细胞一定程度的损害,故重度颅脑外伤等因素引起脑血流自动调节机制不全时进行AHH应谨慎。     

氟比洛芬酯预先给药对全脑缺血再灌注大鼠血脑屏障通透性的影响

目的 探讨氟比洛芬酯预先给药对全脑缺血再灌注大鼠血脑屏障通透性的影响.方法 健康雄性SD大鼠45只,体重300～350 g,随机分为3组(n=15):假手术组(S组)、缺血再灌注组(IR组)和氟比洛芬酯预先给药组(F组).采用夹闭双侧颈总动脉联合低血压法建立全脑缺血再灌注模型.S组仅分离双侧颈总动脉,不结扎;IR组、F组于脑缺血前15 min经右颈总静脉分别注射氟比洛芬酯空白乳剂1 ml/kg(容量与F组一致)、氟比洛芬酯10 mg/kg.再灌注24 h时,静脉注射伊文思蓝(EB)3 ml/kg.取脑组织,观察病理学结果,测定神经元凋亡率、脑含水量、脑组织EB、TNF-α、IL-1β及IL-10的含量.结果 与S组比较,IR组和F组神经元凋亡率、脑含水量、脑组织EB、TNF-α、IL-1β及IL-10含量升高(P＜0.05或0.01);与IR组比较,F组神经元凋亡率、脑含水量和脑组织EB、TNF-α和IL-1β的含量降低,IL-10含量升高(P＜0.05或0.01).F组脑组织病理学损伤较IR组减轻.结论 氟比洛芬酯预先给药可降低全脑缺血再灌注大鼠血脑屏障通透性,减轻脑损伤,其机制可能与抑制炎性反应有关.     

脂氧素A4对局灶性脑缺血再灌注大鼠血脑屏障通透性的影响

目的 探讨脂氧素A4对局灶性脑缺血再灌注大鼠血脑屏障通透性的影响.方法 健康成年雄性SD大鼠54只,体重200～250 g,随机分为3组(n=18):假手术组(S组)、局灶性脑缺血再灌注组(I/R组)和脂氧素A4组(L组).采用改良线栓法制备大鼠局灶性脑缺血再灌注损伤模型,阻断右侧大脑中动脉缺血2 h后行再灌注.L组缺血即刻右侧侧脑室注射脂氧素A4 100 ng,S组和I/R组右侧侧脑室注射等容量生理盐水5 μl.于再灌注24 h时行神经功能缺陷评分,静脉注射2%伊文斯蓝4 ml/kg,1 h后处死大鼠取脑,测定右侧脑水含量和伊文斯蓝含量,检测脑皮质基质金属蛋白酶9(MMP-9)的表达.结果 与S组比较,I/R组和L组神经功能缺陷评分、脑水含量和伊文斯蓝含量升高,脑皮质MMP-9表达上凋(P＜0.05或0.01);与I/R组比较,L组神经功能缺陷评分、脑水含量和伊文斯蓝含量降低,脑皮质MMP-9表达下调(P＜0.01).结论 脂氧素A4可降低血脑屏障通透性,减轻脑水肿,促进局灶性脑缺血再灌注损伤大鼠的神经功能恢复,其机制与抑制MMP-9表达上调有关.     

高碳酸血症对严重低氧缺血大鼠脑损伤的影响

目的研究高碳酸血症对严重低氧缺血大鼠脑损伤的影响及其机制。方法雄性SD大鼠48只,随机分为假手术组(S组)、低氧缺血组(HI组)和高碳酸血症组(HP组),每组16只。S组暴露左侧颈总动脉但不结扎,1h后机械通气,维持PaO_2和PaCO_2在正常水平3h。制作低氧缺血模型,HI组吸入11%~13%O_2并维持PaO_230~49mm Hg;HP组在HI组的基础上吸入11%~13%O_2-8%CO_2-N2混合气维持PaO_230~49mm Hg,PaCO_260~80mm Hg。机械通气3h后处死大鼠,观察脑组织水肿及病理改变,采用TUNEL法检测皮质神经元凋亡,应用FITC-dextran检测血脑屏障通透性的变化,免疫荧光法检测皮质水通道蛋白4(AQP4)及缺血区皮质内皮细胞的标记物(RECA-1)的表达,Western blot法检测AQP4的蛋白含量变化。结果与S组比较,HI组和HP组血脑屏障通透性明显升高,脑含水量明显增加(P0.05);与HI组比较,HP组脑含水量明显增加(P0.05),脑组织损伤加重,TUNEL染色阳性细胞数明显增加(P0.05),脑皮质AQP4蛋白含量明显升高,RECA-1荧光强度明显降低,断离现象明显增多,血脑屏障通透性明显增加(P0.05)。结论高碳酸血症加重了严重的低氧缺血性脑损伤,其机制可能与脑皮质AQP4蛋白表达的增加和血脑屏障的破坏有关。     

异丙酚预先给药对甘露醇诱导大鼠高渗性血脑屏障损伤的影响

目的观察不同剂量异丙酚预先给药对甘露醇诱导大鼠高渗性血脑屏障损伤的影响。方法24只健康、雄性SD大鼠随机分为三组(n=8):对照组(C组)、小剂量异丙酚组(P1组)和大剂量异丙酚组(P2组)。经大鼠颈内动脉以0.25 ml·kg-1·s-1的速率注射20%甘露醇30 s建立血脑屏障损伤模型,在血脑屏障损伤前,P1组和P2组分别经股静脉注射异丙酚20、40 mg·kg-1,以14C-a-氨基异丁酸(14C-AIB)和3H-葡聚糖(3H-dextran)作为同位素示踪物,在血脑屏障开放后取血及脑组织标本测定同位素放射活性,计算14C-AIB的血/脑转运系数(Ki)。结果C组、P1组和P2组应用甘露醇同侧大脑皮质的Ki分别是相应对侧大脑皮质的4.9、3.5和2.5倍(P<0.01),与C组同侧大脑皮质Ki比较, P2组降低47%(P<0.05),三组间对侧大脑皮质Ki比较差异无统计学意义。C组同侧大脑皮质的血浆容量高于对侧大脑皮质。结论大剂量异丙酚预先给药对甘露醇诱导大鼠高渗性血脑屏障损伤具有保护作用。     

Effect of dexamethasone by local treatment on cerebral edema and serum myelin basic protein after brain injury in rabbits

ＳＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ ,ＴｈｅＦｉｒｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌ,ＨｅｎａｎＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｚｈｅｎｇｚｈｏｕ 45 0 0 5 2 ,Ｃｈｉｎａ (ＹａｎｇＢａｎｄＳｏｎｇＬＪ)ＡｌｂｅｒｔＥｉｎｓｔｅｉｎＣｏｌｌｅｇｅｏｆＭｅｄｉｃｉｎｅｏｆＹｅｓｈｉｖｅＵｎｉｖｅｒｓｉｔｙ ,ＮｅｗＹｏｒｋ ,10 46 1(ＧｕａｎＦＸ)ＴｈｅＰｈｙｓｉｃｓＤｅｐａｒｔｍｅｎｔｏｆＨｅｎａｎＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｚｈｅｎｇｚｈｏｕ 45 0 0 5 2 ,Ｃｈｉｎａ (Ｌｉ…     

Spironolactone in preventing hypokalemia following traumatic brain injury

Objective： Hypokalemia is a frequent complication observed after traumatic brain injury （TBI）.We evaluated the effect of spironolactone on preventing hypokalemia following moderate to severe TBI.Methods： Patients with moderate to severe TBI, whose Glasgow Coma Scale （GCS） scores of 9-12 and ＜9,respectively, were equally randomized into intervention and control groups, matching with severity of trauma and baseline serum level of potassium. For the intervention group, we administrated spironolactone （1 mg/kg per day）on the second day of admission or the first day of gavage tolerance and continued it for seven days. No additional intervention was done for controls. Hypokalemia （mild： 3-3.5 mg/L, moderate： 2.5-3 mg/L, and severe： ＜2.5 mg/L serum K＋） and other electrolyte abnormalities were compared between the two groups at the end of the intervention.Results： Sixty-eight patients （58 males and 10 females）were included with mean age=（33.1±11.8） years, and GCS=7.6±2.8. The two groups were similar in baseline characteristics.Patients who received spironolactone were significantly less likely to experience mild, moderate, or severe hypokalemia （8.8%, 2.9%, and 0） compared with controls （29.4%, 11.7%,and 2.9%, respectively, P＜0.05）. No significant difference was observed between the two groups in the occurrence of other electrolyte abnormalities, hyperglycemia or oliguria.Conclusion： Spironolactone within the first week of head injury could prevent the occurrence of late hypokalemia with no severe side effects.     

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.     

Pathophysiological and pathochemical aspects of cerebral edema

Conclusions and summary Cerebral edema is an increase in brain water content causing expansion of cerebral tissue volume. There are two different entities of cerebral edema occurring alone or together. Formation of vasogenic brain edema requires breakdown of the blood-brain barrier, while cytotoxic edema forms by alterations of the permeability of cell membranes, and/or disturbances of active, energy-dependent transport. In primaryvasogenic edema, a secondary cytotoxic component is always observed, while conversely, secondary vasogenic edema is usually not found in primarycytotoxic edema. Ischemic brain edema may be an exception.The mechanism of barrier breakdown in vasogenic edema is still open to debate. Patency of endothelial junctions has rarely been found, whereas enhanced formation of endothelial vesicles is frequently encountered. The problem remains that the direction of vesicular transport in those conditions has not been worked out clearly enough. Nevertheless, this point merits particular efforts because vesicular transport may serve as a target for more effective methods of edema treatment.Investigations to improve the understanding of the role of brain edema factors in edema formation and persistence are in line with this argument. Release of glutamate from damaged cells into the extracellular compartment and activation of the plasma kininogen-kinin system in vasogenic edema are particularly attractive models among the many candidates singled out for investigation. Progress in the brain edema problem can also be expected when the mechanism of glial and nerve cell swelling is better understood.Studies on resolution of vasogenic edema provided insight into the problem of how brain tissue manages to regain control over its extracellular environment. Cellular uptake, retrograde pinocytosis, and probably most important, drainage into the CSF system are the current concepts. Although swelling of nerve and glial cells, myelin splitting, pollution of the extracellular space by an abnormal fluid can be considered to interfere with normal brain function, brain edema is above all a space-occupying process causing rise of intracranial pressure, eventually leading to reduction of cerebral blood flow, and distortion and herniation of vital parts of the brain. Both cerebral ischemia and brain tissue herniation may finally determine whether a patient will survive this condition. It is therefore not surprising that the most powerful methods of brain edema treatment, as for example hypertonic solutions, do not specifically affect the edema proper, but rather the rise in intracranial pressure. We should become aware that, apart from corticosteroids, most of the therapeutic methods currently in use have not been shown to interfere with specific aspects of brain edema, such as permeability of the blood-brain barrier, primary or secondary swelling of cells, edema factors, or resolution of edema. We may be confident, however, that an increased understanding of such aspects will ultimately benefit edema treatment.The technical and secretarial help of Hedwig Kuschke, Beate Komarek and Mechthild Stein is gratefully acknowledged.Dedicated to Professor Anthonie Van Harreveld on the occasion of his 75th birthday.     

Neuroprotective effects of progesterone in traumatic brain injury: blunted in vivo neutrophil activation at the blood-brain barrier

Background

Progesterone (PRO) may confer a survival advantage in traumatic brain injury (TBI) by reducing cerebral edema. We hypothesized that PRO reduces edema by blocking polymorphonuclear (PMN) interactions with endothelium (EC) in the blood-brain barrier (BBB).

Methods

CD1 mice received repeated PRO (16 mg/kg intraperitoneally) or vehicle (cyclodextrin) for 36 hours after TBI. Sham animals underwent craniotomy without TBI. The modified Neurological Severity Score graded neurologic recovery. A second craniotomy allowed in vivo observation of pial EC/PMN interactions and vascular macromolecule leakage. Wet/dry ratios assessed cerebral edema.

Results

Compared with the vehicle, PRO reduced subjective cerebral swelling (2.9 ± .1 vs 1.2 ± .1, P < .001), PMN rolling (95 ± 1.8 vs 57 ± 2.0 cells/100 μm/min, P < .001), total EC/PMN adhesion (2.0 ± .4 vs .8 ± .1 PMN/100 μm, P < .01), and vascular permeability (51.8% ± 4.9% vs 27.1% ± 4.6%, P < .01). TBI groups had similar a Neurological Severity Score and cerebral wet/dry ratios (P > .05).

Conclusions

PRO reduces live pericontusional EC/PMN and BBB macromolecular leakage after TBI. Direct PRO effects on the microcirculation warrant further investigation.     

Effect of intracranial pressure and cerebral perfusion pressure on outcome prediction of severe traumatic brain injury

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