脑出血患者血肿周围脑组织中P75NTR、TrkA的表达及其与细胞凋亡的关系

目的 通过对人脑出血后血肿周围不同区域组织中的P75NTR、TrkA表达的检测,探讨其在脑出血后血肿周围组织细胞凋亡中的作用. 方法采集脑出血血肿清除术患者的脑组织标本,分别运用DNA断裂原位末端标记(TUNEL)法及免疫组化技术检测血肿周围及远隔部位组织中细胞凋亡率与P75NTR、TrkA的表达. 结果相对于远隔部位组织,脑出血后血肿周围组织中的细胞凋亡率与P75NTR的表达水平明显增加(P<0.05),而TrkA的表达水平并没有明显变化(P>0.05).P75NTR的阳性细胞率与TUNEL阳性细胞率呈正相关(r=0.628,p=0.000). 结论脑出血后血肿周围组织中凋亡细胞明显增多,P75NTR介导的细胞凋亡通路可能发挥了重要的作用;TrkA在脑出血发生后并没有增量表达以增加细胞存活,未起到拮抗P75NTR介导的细胞凋亡作用.     

脑出血患者血肿周围脑组织中P75NTR、TrkA的表达及其与细胞凋亡的关系

目的 通过对人脑出血后血肿周围不同区域组织中的P75NTR、TrkA表达的检测,探讨其在脑出血后血肿周围组织细胞凋亡中的作用. 方法采集脑出血血肿清除术患者的脑组织标本,分别运用DNA断裂原位末端标记(TUNEL)法及免疫组化技术检测血肿周围及远隔部位组织中细胞凋亡率与P75NTR、TrkA的表达. 结果相对于远隔部位组织,脑出血后血肿周围组织中的细胞凋亡率与P75NTR的表达水平明显增加(P<0.05),而TrkA的表达水平并没有明显变化(P>0.05).P75NTR的阳性细胞率与TUNEL阳性细胞率呈正相关(r=0.628,p=0.000). 结论脑出血后血肿周围组织中凋亡细胞明显增多,P75NTR介导的细胞凋亡通路可能发挥了重要的作用;TrkA在脑出血发生后并没有增量表达以增加细胞存活,未起到拮抗P75NTR介导的细胞凋亡作用.     

人脑出血血肿周围组织中神经生长因子前体-神经营养因子受体p75-sortilin通路与细胞凋亡

This study demonstrated that brain areas surrounding the site of hematoma following intracerebral hemorrhage are characterized by significantly increased apoptosis and expression of neurotrophin receptor p75 and sortilin. However, as detected by terminal deoxynucleotidyl transferase dUTP nick end labeling and immunohistochemical staining, there was no significant change in nerve growth factor precursor expression levels. The appearance of neurotrophin receptor p75 expressing cells was positively correlated with cells that were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. These findings confirm that the nerve growth factor precursor-neurotrophin receptor p75-sortilin heterotrimeric complex-mediated apoptosis pathway may play an important role in cellular apoptosis following intracerebral hemorrhage.     

高血压性脑出血血肿周围脑组织细胞间粘附分子-1的表达

目的探讨急性高血压性脑出血患者细胞间粘附分子-1(ICAM-1)在血肿周围脑组织和正常脑组织中的表达及其意义。方法选择30例行开颅手术治疗的急性高血压性脑出血患者,采用免疫组化技术检测ICAM-1在血肿周围脑组织及正常脑组织中的表达。结果实验组血肿周围脑组织可见ICAM-1的表达水平上调,其表达水平明显高于正常脑组织的表达水平(P<0.01)。神经元和血管内皮细胞共同表达ICAM-1,且神经元表达较明显。结论ICAM-1在人类高血压性脑出血血肿周围脑组织的表达水平上调,其表达上调可能参与了血肿周围脑组织的白细胞浸润,最终引发炎性反应和继发性脑损伤。     

人脑出血后proNGF、sortilin的表达及与细胞凋亡的关系

目的研究人脑出血后神经生长因子前体（proNGF）、sortilin在血肿周围组织中的表达及与细胞凋亡的关系。方法本实验采集临床手术患者的脑组织标本,利用末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸生物素原位缺口末端标记法（TUNEL）检测血肿周围组织中的凋亡细胞,运用免疫组化技术检测血肿周围组织及远隔部位组织中proNGF、sortilin的表达。结果脑出血后血肿周围组织中细胞凋亡率明显增高（P〈0.01）,proNGF的表达水平并没有显著变化（P〉0.05）,而sortilin的表达水平则明显增加（P〈0.01）,并且sortilin的表达水平与细胞凋亡率正相关（R=0.648,P=0.00）。结论sortilin在人脑出血后表达增加,与细胞凋亡正相关,proNGF在脑出血后的表达量并未变化。     

脑出血血肿周围脑组织细胞凋亡与细胞色素C表达的关系

目的 研究脑出血(ICH)患者血肿周围脑组织细胞凋亡与细胞色素C(Cyt-C)表达的关系.方法 选择不同时段行血肿清除术的ICH患者32例,选取手术过程中获得的血肿周围脑组织作为标本,采用TUNEL染色及免疫组织化学技术检测凋亡细胞和Cyt-C表达的变化.结果 ICH超早期组(＜8h)可见明显的TUNEL阳性细胞和Cyt-C阳性细胞;早期组(8～48h)二者均达到高峰;延期组(＞48h)TUNEL阳性细胞仍维持较高表达,而Cyt-C阳性细胞计数开始下降.凋亡细胞与Cyt-C表达呈正相关(r=0.87,P＜0.01).结论 ICH患者血肿周围脑组织中存在细胞凋亡,Cyt-C表达是细胞凋亡过程中的一个关键事件.     

Enhanced pulmonary inflammation following experimental intracerebral hemorrhage

The association between brain damage and respiratory dysfunction has been recognized although mechanistic link between the two is still poorly defined. Intracerebral hemorrhage is accompanied by brain injury, stroke, and parenchymal hematoma formation with surrounding inflammation. Increase intracranial pressure as a result of intracerebral hemorrhage may promote localized activation of cytokines and coagulation system including tissue factor release. However, whether intracerebral hemorrhage triggers inflammation in noncerebral organs has not been elucidated. The aim of the present study was to examine the impact of intracerebral hemorrhage on lung inflammatory response. Intracerebral hemorrhage was induced by stereotaxic intrastriatal administration of bacterial collagenase. Expression of intracellular adhesion molecule-1 (ICAM-1), IKB-alpha, tissue factor, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) was evaluated by Western blot analysis. Our results revealed that intracerebral hemorrhage upregulated expression of ICAM-1 and tissue factor in both brain and lung, whereas it enhanced TNF-alpha and IL-1beta mainly in brain within 6 and 24 h of the brain injury. Levels of IKB-alpha remained unchanged in brain and lung tissues. Appearance of inflammatory markers in the lung was accompanied by morphological pulmonary damage. These data suggest that intracerebral hemorrhage may trigger acute inflammatory response in both brain and lung.     

Mild hypothermia effects on matrix metalloproteinase-9 expression in the perihematomal region of rats following experimental intracerebral hemorrhage

BACKGROUND:Matrix metalloproteinase-9(MMP-9)expression increases with intracerebral hemorrhage,and participates in the pathophysiological processes of secondary brain injury after intracerebral hemorrhage.OBJECTIVE:To investigate the effects of mild hypothermia on MMP-9 expression and brain edema in the perihematomal region of experimental intracerebral hemorrhage rats.DESIGN,TIME AND SETTING:The randomized,controlled experiment was performed at the Central Laboratory of Shandong Provincial Hospital between May and September 2007.MATERIALS:Seventy-two,Wistar,male rats,12-weeks old,were used for this study.Rabbit anti-MMP-9 primary antibody was purchased from Boster,China.METHODS:Wistar rats were equally and randomly divided into normothermia and mild hypothermia groups.The two groups each comprised control,6-hour intracerebral hemorrhage,24-hour intracerebral hemorrhage,48-hour intracerebral hemorrhage,72-hour intracerebral hemorrhage,and 1-week intracerebral hemorrhage subgroups,with six rats in each subgroup.Rat models of intracerebral hemorrhage were established by irtjecting 100 μL of autologous blood into the rat caudate nucleus.Rats in the mild hypothermia group received four hours of local mild hypothermia immediately following the injection.Intracerebral temperature was maintained at(33±0.5)℃.Subsequently,intracerebral temperature was spontaneously recovered at 25℃.Rats in the control subgroup were not injected with autologous blood and received only with intracerebral hemorrhage.MAIN OUTCOME MEASURES:Brain water content and MMP-9 expression surrounding the hematoma region.RESULTS:MMP-9 expression increased at 6 hours,and brain edema reached a peak at 48 hours after intracerebral hemorrhage.MMP-9 expression was significantly decreased in the mild hypothermia group compared with the normothermia group at each time point (P<0.05).CONCLUSION:Mild hypothermia can significantly inhibit MMP-9 overexpression and relieve brain edema following intracerebral hemorrhage.     

Mild hypothermia effects on matrix metalloproteinase-9 expression in the perihematomal region of rats following experimental intracerebral hemorrhage**☆

BACKGROUND： Matrix metalloproteinase-9 （MMP-9） expression increases with intracerebral hemorrhage, and participates in the pathophysiological processes of secondary brain injury after intracerebral hemorrhage.
OBJECTIVE： To investigate the effects of mild hypothermia on MMP-9 expression and brain edema in the perihematomal region of experimental intracerebral hemorrhage rats.
DESIGN, TIME AND SETTING： The randomized, controlled experiment was performed at the Central Laboratory of Shandong Provincial Hospital between May and September 2007.
MATERIALS： Seventy-two, Wistar, male rats, 12-weeks old, were used for this study. Rabbit anti-MMP-9 primary antibody was purchased from Boster, China.
METHODS： Wistar rats were equally and randomly divided into normothermia and mild hypothermia groups. The two groups each comprised control, 6-hour intracerebral hemorrhage, 24-hour intracerebral hemorrhage, 48-hour intracerebral hemorrhage, 72-hour intracerebral hemorrhage, and l-week intracerebral hemorrhage subgroups, with six rats in each subgroup. Rat models of intracerebral hemorrhage were established by injecting 100 μL of autologous blood into the rat caudate nucleus. Rats in the mild hypothermia group received four hours of local mild hypothermia immediately following the injection. lntracerebral temperature was maintained at （33 ± 0.5） ℃. Subsequently, intracerebral temperature was spontaneously recovered at 25 ℃. Rats in the control subgroup were not injected with autologous blood and received only with intracerebral hemorrhage.
MAIN OUTCOME MEASURES： Brain water content and MMP-9 expression surrounding the hematoma region. RESULTS： MMP-9 expression increased at 6 hours, and brain edema reached a peak at 48 hours after intracerebral hemorrhage. MMP-9 expression was significantly decreased in the mild hypothermia group compared with the normothermia group at each time point （P 〈 0.05）.
CONCLUSION： Mild hypothermia can significantly inhibit MMP-9 overexpression and reliev     

SHR大鼠脑出血急性期氨氯地平血压干预和血肿周围水肿的相关性研究

目的采用自发性高血压大鼠(SHR)脑出血模型,研究脑出血后急性期血压和血肿周围水肿的相关性。方法胶原酶法制备SHR大鼠脑出血模型,出血部位为右侧基底节区。动物随机分为脑出血组、脑出血常规剂量氨氯地平降压组、脑出血强化剂量氨氯地平降压组。MRI检查并计算血肿周围水肿大小;免疫组化及荧光定量PCR法检测血肿周围水肿的AQP4表达。结果 (1)氨氯地平治疗组MRI检测值显示,脑血肿周围水肿减轻,降压组均优于未干预组,强化降压组优于常规降压组,差异有统计学意义,第3、5、7天的F值分别为16.987、35.448、37.174(P<0.05);收缩压降低幅度和血肿周围水肿体积之间有相关性,在第3、5、7天的相关系数r分别为0.83、0.89、0.83,P=0.000;舒张压降低幅度和血肿周围水肿体积之间有相关性,在第3、5、7天的相关系数r分别为0.82、0.89、0.84,P=0.000)。(2)降压组血肿周围水肿的AQP4表达下调均优于未干预组,强化降压组优于常规降压组,差异有统计学意义,第3、5、7天的F值分别为217.058、21、51.706(P<0.05)。结论 (1)氨氯地平有效降压能使脑出血血肿周围水肿缩小;(2)氨氯地平可能通过抑制AQP4表达促使血肿周围脑水肿减轻;(3)收缩压、舒张压的升高均可促使血肿周围脑水肿扩大。     

Effects of basic fibroblast growth factor on superoxide dismutase activity and malondialdehyde content in the rat brain following intracerebral hemorrhage

BACKGROUND: Studies have confirmed that basic fibroblast growth factor (bFGF) promotes neuronal survival and neurite outgrowth. OBJECTIVE: To compare and verify the effects of bFGF on superoxide dismutase activity and malondialdehyde content in rat brain tissues surrounding a hemorrhagic lesion, as well as the hippocampus at the hemorrhagic side. DESIGN, TIME AND SETTING: The randomized, controlled, neurobiological study was performed at the Science Experimental Center and Research Laboratory, Guangxi Medical University, China, from September to December 2006. MATERIALS: Ninety-two adult, healthy, Wistar rats of equal gender were used to establish intraeerebral hemorrhage by infusing type VII collagenase into the left internal capsule. Type Ⅶ collagenase (Sigma, USA), superoxide dismutase and malondialdehyde kits (Jiancheng, China), and bFGF (Institute of Bioengineering, Ji'nan University, China) were used for this study. METHODS: Ninety successfully lesioned rats were equally and randomly divided into three groups. Rats in the bFGF group were intramuscularly injected daily with bFGF (8μg/kg). Rats in the saline control group received an equal volume of saline. The rats in the model group did not receive other interventions. Superoxide dismutase activity was measured using the xanthine oxidase method. Malondialdehyde contents were detected using the thiobarbituric acid method. MAIN OUTCOME MEASURES: At 1, 3, and 7 days following intracerebral hemorrhage, superoxide dismutase and malondialdehyde were determined in the brain tissue surrounding the hematoma and in the hippocampus in the affected hemisphere. RESULTS: In brain tissue surrounding the hematoma, superoxide dismutase activity was significantly increased in the bFGF group at 3 and 7 days after intracerebral hemorrhage compared with the saline control group, whereas malondialdehyde content was significantly decreased (P < 0.05). In the hippocampus, superoxide dismutase activity was significantly increased in the bFGF group at 7 days following intracerebral hemorrhage compared with the saline control group, whereas malondialdehyde content was significantly decreased (P < 0.05). At 1, 3, and 7 days after intracerebral hemorrhage, there was no significant difference between the saline control group and the model group with regards to parameter or brain region (P > 0.05). CONCLUSION: Increased superoxide dismutase activity and decreased malondialdehyde content were detected in tissue surrounding the hematoma, as well as the ipsilateral hippocampus, of intracerebral hemorrhage rats treated with bFGF. Changes in these parameters were detected earlier in tissue adjacent to the lesion, compared with the ipsilateral hippocampus.     

大鼠脑出血后血肿周围区神经元胀亡及3-AB对其胀亡、凋亡的影响

目的 通过建立大鼠脑出血动物模型,观察大鼠脑出血后血肿周围区神经元胀亡时程、分布变化规律及3.氨基苯甲酰胺(3-AB)对神经元胀亡、凋亡的影响.方法 成年健康Wistar大鼠84只随机分为脑出血+3-AB组(A组)、脑出血组(B组)、对照组(C组).A、B组脑尾壳核注入自体血50μl,A组3-AB腹腔注射干预.分别于术后6h、1d、2d、3d、5d、7d处死.根据Rosenberg法对各组大鼠进行神经功能评分;在光、电镜下观察神经元胀亡随时间、空间的变化规律;Caspase-3免疫组化,探讨3-AB对其胀亡和凋亡的影响.结果 脑出血大鼠神经功能评分在24h最高;血肿周围神经元出现胀亡和凋亡;胀亡指数在24h达高峰,此后逐渐下降,3组比较有统计学差异.凋亡亦在24h达高峰,Caspase-3阳性神经元数目3组相比有统计学意义.结论 脑出血后血肿周围神经元胀亡和凋亡共存;胀亡随时间、空间变化而呈规律性改变;3-AB能抑制其胀亡,促进凋亡.     

高血压脑出血患者血肿灶周组织形态学观察

目的 观察高血压脑出血患者急性期血肿周围组织的病理变化.方法 将28例高血压脑出血患者微创技术治疗时吸出的脑组织进行HE和刚果红染色.结果 光镜下可见大片出血病灶和点状出血,部分小动脉玻璃样变性及粟粒型动脉瘤;血管周围可见嗜中性粒细胞渗出,血管腔内充血,脑组织水肿,神经胶质细胞及神经元均有不同程度的坏死.同时通过CT影像学改变进行对比观察血肿发生部位与病理变化关系.结论自发性的高血压性脑出血及脑动脉扩张与动脉血管发生玻璃样变性有关,少数与动脉急性坏死、微动脉瘤、细动脉粥样硬化、淀粉样变性有关.通过CT进一步证实高血压动脉硬化性脑出血部位以基底节最为常见,而血管淀粉样变性导致的脑出血主要以脑叶为主.     

Homocysteine aggravates cerebral hemorrhage in rats Correlation with oxygen-free radical production and cell apoptosis in tissue surrounding hematoma

BACKGROUND:Previous studies have demonstrated that homocystaine is an independent risk factor for ischemic stroke,as determined by detection of apoptosis and oxygen-free radical scavengers following cerebral ischemia.However,the mechanisms of homocysteine remain unclear.Several reports have addressed the effects of homocysteine on ischemic stroke.OBJECTIVE:To analyze the effects of homocysteine on apoptosis,intracellular superoxide dismutase(SOD)activity,and malondialdehyde content in tissue surrounding hematoma in rats with cerebral hemorrhage,and to determine the action pathway of malondialdehyde following cerebral hemorrhage.DESIGN,TIME AND SETTING:The randomized,controlled,animal experiment was performed at the Laboratory of Molecular Biology,Hospital Affiliated to Luzhou Medical College,China from April 2007 to April 2008.MATERIALS:In situ apoptosis detection kit(Roche,Mannheim,Germany),SOD detection kit and malondialdehyde detection kit(Nanjing Jiancheng Bioengineering Institute,China),and homocysteine(Sigma,St Louis,MO,USA)were used in the present study.METHODS:A total of 75 Sprague Dawley rats were equally and randomly assigned to sham surgery,model,and homocysteine groups.Autologous blood was infused into the caudate putamen of rats to establish models of cerebral hemorrhage in model and homocysteine groups.Homocysteine was injected directly into the brain through the skull at the hematoma hemisphere at 30 minutes after model induction in the homocysteine group.MAIN OUTCOME MEASURES:At 6,12,24,and 72 hours,as well as 1 week,post-surgery,neurological deficits were observed in each group.Brain water content was measured using the dry-wet weight method.Cell apoptosis in tissue surrounding the hematoma was detected utilizing terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling(TUNEL).SOD activity and malondialdehyde content in tissue surrounding the hematoma were respectively measured using the xanthine oxidase and thiobarbituric acid methods.RESULTS:Neurological function was similar between model and homocysteine groups following cerebral hemorrhage(P> 0.05).Brain water content was increased at 12 hours post-surgery,peaked at 3 days,and remained unchanged at 7 days in the model group.Brain edema was not significantly aggravated following homocysteine intervention(P > 0.05),but SOD activity significantly decreased and malondialdehyde content significantly increased(P < 0.05).The number of apoptotic cells increased in rats with cerebral hemorrhage at 12 hours(P< 0.05),and numbers peaked at 72 hours following model establishment(P< 0.05).The time of peak value was identical between model and homocysteine groups.Brain water content was negatively associated with SOD activity(rmodel group =-0.448,P < 0.05; rhomocysteine group =-0.612,P < 0.05),but was positively associated with malondialdehyde content(rmodel group = 0.542,P < 0.05; rhomccysteine group=0.684,P < 0.05)in brain tissues surrounding the hematoma following surgery in model and homocysteine groups.CONCLUSION:Homocysteine aggravates neurological dysfunction and brain edema in rats with cerebral hemorrhage.The mechanisms of action are likely associated with production of oxygen-free radical and cellular apoptosis following cerebral hemorrhage.     

同型半胱氨酸对大鼠脑出血后血肿周围细胞凋亡及Caspase-3表达的影响

目的本实验通过观察同型半胱氨酸(Hcy)对脑出血模型大鼠血肿周围神经细胞凋亡和Caspase-3的表达的影响,探讨实验性脑出血后Hcy的损伤作用及其机制,并为预防及治疗脑出血提供实验理论基础。方法应用立体定向技术制备脑出血模型,Hcy组于术后30min予血肿同侧颅内直接注射Hcy,固定后连续切片作TUNEL染色和Caspase-3免疫组化染色,数据用SPSS13.0统计分析。结果假手术组偶可见TUNEL细胞表达,Caspase-3少量表达;脑出血组6h血肿周边组织出现TUNEL阳性细胞,72h达高峰,Caspase-3在脑出血后6h表达开始增高,24h达到高峰,应用Hcy干预后自12h起各时间点TUNEL细胞和Caspase-3表达均较ICH组增加(P<0.05),以各自高峰时间最为显著(P<0.05),但未能改变TUNEL细胞和Caspase-3表达的高峰时间。结论脑出血后血肿周围细胞凋亡与Caspase-3表达有关,Caspase-3介导了细胞凋亡的发生。Hcy能够促进脑出血后的细胞凋亡,可能与诱导Caspase-3表达有关,进一步证实Hcy为脑血管疾病的独立危险因素之一。     

自发性脑出血早期血肿扩大首诊CT分析

探讨首诊头部CT影像对自发性脑出血早期血肿扩大的预测价值。300例发病后6h内入院的自发性脑出血患者,经CT检查显示其中61例(20.33%)发生早期血肿扩大,经单因素和多因素Logistic回归分析显示,早期血肿扩大与首诊CT距发病时间短、血肿密度不均匀、中至重度脑萎缩及血     

脑出血后IGF-1在脑组织中的表达及其对细胞凋亡的影响

目的研究胰岛素样生长因子-1（IGF-1）在实验性大鼠脑出血后脑组织中的表达厦其对细胞凋亡的影响。方法应用立体定向技术，将自体未抗凝血注入大鼠基底节区以制备脑出血模型；将动物分为正常对照组、实验组厦干预组，分别在不同时间断头取脑以制作标本，连续切片分别作IGF-1阳性细胞免疫组化染色及TUNEL染色。结果脑出血后2h血肿周围脑组织表达IGF-1，24h达表达高峰，7d时恢复正常；TUNEL染色阳性细胞于脑出血后8h开始出现，3d时达高峰，7d时仍有表达；给予外源性IGF-1后，凋亡细胞显著减少，与同时点实验组相比，差别有显著性。结论脑出血后IGF-1可抑制细胞凋亡的发生，从而减轻脑出血后继发性脑损伤。     

Increased Expression of Small Heat Shock Protein αB-crystallin After Intracerebral Hemorrhage in Adult Rats

αB-crystallin (αBC) is involved in diverse cellular activities. Previous studies demonstrated that αBC had anti-apoptotic and proliferation-promoting effects in multiple diseases. Here, we explored the αBC’s roles in the pathophysiology of intracerebral hemorrhage (ICH). An ICH rat model was established and assessed by behavioral tests. Using Western blot and immunohistochemistry, significant up-regulation of αBC was found in neurons and astrocytes in brain areas surrounding the hematoma following ICH. Increase of αBC expression was found to be accompanied by the increased expression of proliferating cell nuclear antigen (PCNA), p53, Bax, and active-caspase-3. αBC was co-localized with PCNA in astrocytes or active-caspase-3 in neurons, suggesting its role in astrocyte proliferation and neuronal apoptosis. Our in vitro study, using αBC RNA interference in PC12 cells, indicated that αBC might exert its anti-apoptotic function in neuronal apoptosis. Thus, αBC may play a role in protecting the brain from secondary damage following ICH.     

米诺环素早期干预脑出血：对大鼠脑内血管内皮生长因子、神经生长因子、热休克蛋白70表达及血脑屏障通透性的影响

Abstract Inflammatory factor aggregation and blood-brain barrier (BBB) damage occur around hematoma foci following intracerebral hemorrhage. Minocycline is lipophilic, can pass through the BBB, and shows anti-inflammatory effects in models of central nervous system disease. We found that minocycline application at 6 hours after intracerebral hemorrhage reduced BBB permeability, decreased vascular endothelial growth factor expression, and increased nerve growth factor and heat shock protein 70 expression, primarily in neurons and microglia. Early intraperitoneal injection of minocycline attenuated BBB damage possibly by reducing vascular endothelial growth factor expression and enhancing nerve growth factor and heat shock protein 70 expression. Key Words: blood-brain barrier; intracerebral hemorrhage; vascular endothelial growth factor; nerve growth factor; heat shock protein 70; therapy     

Electrocardiogram changes during hematoma enlargement in intracerebral hemorrhage patients**☆

BACKGROUND： It has been reported that cerebrovascular disease causes changes in electrocardiogram results. OBJECTIVE： To investigate changes in electrocardiogram results in patients with intracerebral bematoma enlargement. DESIGN, TIME AND SETTING： The present case-retrospective analysis study was performed at the Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology from January 2005 to October 2006. PARTICIPANTS： A total of 225 intracerebral hemorrhage patients （142 males and 83 females） that were hospitalized at the Department of Neurology were enrolled the present study. The patient selection was in accordance with diagnostic criteria from the Fourth National Cerebrovascular Disease Congress of China in 1995, and diagnosis was confirmed using computed tomography. All patients underwent computed tomography twice within 24 hours following intracerebral hemorrhage, and were subjected to electrocardiogram examination after admission. METHODS： According to hematoma enlargement following intracerebral hemorrhage, all patients were divided into hematoma enlargement （n = 20） and non-hematoma enlargement （n = 205） groups. Because of the large patient number difference between the two groups, the hematoma enlargement group was matched with the non-hematoma enlargement group. Patients meeting these conditions were included in the non-hematoma enlargement group. Finally, 75 patients were included in the final analysis, 19 in the hematoma enlargement group and 56 in the non-hematoma enlargement group. Clinical data from the two groups were statistically analyzed. MAIN OUTCOME MEASURES： The incidence of electrocardiographic abnormalities between the hematoma enlargement and non-hematoma enlargement groups. RESULTS： In the hematoma enlargement group, 15 patients （79%） developed electrocardiographic abnormafities. In the non-hematoma enlargement group, 24 patients （43%） presented with electrocardiographic abnormalities. There were sig