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1.
目的 研究高血压脑出血患者血肿周边是否存在"半暗带"区;以及"半暗带"出现的时间和空间规律.方法 根据"半暗带"区的灌注标准和代谢标准,对符合人选标准的高血压脑出血患者,于发病后1、3、5、25d采用动态核磁共振(MRI)评定,获取所需的弥散、灌注和波谱等观察数据.结果 高血压脑出血患者发病后1、3、5、25d,用灌注标准或代谢标准评定都存在有"半暗带";"半暗带"呈斑片状分布在血肿周围;"半暗带"可位于血肿周边上、下、前、后、内、外侧等方向,其中位于血肿内侧多见.1例患者血肿周边"半暗带"演变为脑梗死灶.结论 高血压脑出血患者血肿周围存在斑片状"半暗带";"半暗带"存在于研究的各时间点,以血肿内侧多见.  相似文献   

2.
1引言 业已证实,低温在急性局灶性和全脑缺血实验模型中具有神经保护作用。尽管其神经保护机制尚待完全阐明,但低温能影响脑缺血过程的多种病理生理学机制。缺血核心(不可逆性受损的神经元)及其周围低灌注区(即“缺血半暗带”)的概念已被广泛接受。尽管缺血半暗带内的神经元出现功能障碍,但如能及时恢复灌注,仍可恢复正常。  相似文献   

3.
大鼠脑挫裂伤半暗带水肿与血-脑屏障破坏的关系   总被引:1,自引:0,他引:1  
目的研究大鼠局灶性脑挫裂伤半暗带的水肿变化与血-脑屏障(BBB)破坏的关系。方法将126只雄性SD大鼠随机分为3组:假手术组、挫裂伤组和给药组,采用Feeney法制作脑挫裂伤模型,给药组采用曲克芦丁脑蛋白水解物合剂腹腔给药,分别用伊文思蓝(EB)染色法和干湿法观察BBB的变化和脑组织的水肿情况,同时电镜观察超微结构。结果EB染色显示:挫裂伤组和给药组在伤后1 h EB开始漏出,6 h最严重。水含量测定结果显示:挫裂伤组和给药组伤后6 h水含量开始增加,72 h增至高峰。与挫裂伤组比较,给药组脑组织EB溢出量、水含量降低(P<0.05)。结论大鼠脑挫裂伤半暗带BBB通透性改变早于脑水肿的发生,提示BBB破坏可能是早期创伤性脑水肿的结构基础。曲克芦丁脑蛋白水解物合剂可通过改善BBB等多种途径治疗脑挫裂伤。  相似文献   

4.
目的 研究丁苯酞软胶囊对急性脑梗死患者缺血半暗带的影响.方法 61例急性脑梗死(病程<6h)患者随机分为丁苯酞组与对照组;在脑梗死常规治疗的基础上,丁苯酞组加用丁苯酞软胶囊0.2g口服4次/d.两组患者分别在治疗前及治疗后12 h进行CT灌注成像检查,观察并比较两组缺血低灌注区及缺血中心区的面积;以及两组患者治疗后缺血低灌注改善、梗死区未扩大和存在缺血半暗带的比率.结果 治疗后,丁苯酞组的缺血低灌注面积[(1630.71±1094.23) mm2]、缺血中心区面积[(811.35±1038.14)mm2]均显著小于对照组[(3233.77±1117.67) mm2,(1661.5±1035.34) mm2](均P<0.05);丁苯酞组缺血低灌注区缩小(77%)、梗死区无扩大(52%)及存在缺血半暗带(71.43%)的比率均分别显著高于对照组(53%,20%,37.93%)(均P<0.05).结论 丁苯酞软胶囊能明显改善急性脑梗死患者的脑缺血低灌注,延长半暗带组织的存活时间,挽救缺血半暗带组织;并避免缺血梗死区扩大.  相似文献   

5.
目的探讨表观弥散系数(ADC)图在诊断急性脑梗死缺血半暗带中的价值。方法对27例发病时间在1~6h的超急性脑梗死患者行常规MRI、磁共振弥散加权成像(DWI)和磁共振灌注加权成像(PWI)确定缺血半暗带的范围,计算梗死中心区、IP区及对侧镜像区的ADC比值和相对ADC值(rADC)值并加以比较。结果在27例超急性脑梗死患者中,25例患者病灶区ADC值明显下降;21例患者PWI>DWI,其病灶中心rADC值与IP区相比显著下降。结论ADC图可以反映脑组织的损伤程度,通过测量脑梗死病灶中心区和边缘区rADC值可以判断缺血半暗带的存在。  相似文献   

6.
急性脑梗死缺血半暗带演变的磁共振成像研究   总被引:1,自引:0,他引:1  
目的:探讨应用磁共振弥散/灌注成像技术判断急性脑梗死后缺血半暗带IP存在的范围和时间规律。方法:对72例发病时间在1~24h的急性脑梗死患者行常规MRI、磁共振弥散加权成像(DWI)和磁共振灌注加权成像(PWI)确定IP的范围,计算梗死中心区、IP区及对侧镜像区的ADC值和rADC值并加以比较。结果:26例发病时间〈6h的患者PWI显示存在低灌注区者,其中PWI〉DWI者21例,30例发病时间在6~24h的患者PWI显示存在低灌注区者,其中PWI〉DWI者2例;PWI〉DWI者病灶中心ADC值与IP区及对侧镜像区ADC值差异有统计学意义,其IP区ADC值与其对侧镜像区差异无统计学意义。结论:DWI和PWI结合能灵敏的判断IP的存在,IP存在的时间窗有一定的个体差异。  相似文献   

7.
目的探讨CT灌注成像(CT perfusion imaging,CTPI)对急性缺血性脑卒中半暗带的评估。方法应用16层螺旋CT对21例急性缺血性脑卒中患者行CTPI检查,于1w后复查CTPI,分析梗死区和半暗带的相对脑血流量(relative cerebral blood flow,rCBF)、相对脑血容量(relative cerebralvolume,rCBV)的数值变化,评估半暗带。结果所有患者的灌注CT图像皆有明确的异常灌注区,病灶中CBF下降,CBV下降或正常,MTT明显延长。梗死区rCBF、rCBV无变化(P>0.05),相对血流量及相对血容量极低;而半暗带区治疗前后rCBF明显改善(P<0.05)、rCBV变化不明显(P>0.05),半暗带区rCBF的可信区间为0.425~0.582。结论CTPI能够对半暗带进行判定,并指导临床的进一步治疗。  相似文献   

8.
缺血半暗带代表的是缺血后虽已丧失电活动但仍能维持电位和跨膜离子电位的、并且可存活一段时间的部分脑组织.目前,多数学者认为缺血半暗带是位于严重缺血中心周围低灌注的缺血区,该区随缺血时间的长短而处于动态变化过程中,若能及时恢复血供则可转化为正常灌注区,否则将发展为不可逆的梗死.因此,围绕早期明确缺血半暗带的临床与基础研究对于急性缺血性脑卒中的治疗具有重要指导意义.  相似文献   

9.
灌注及弥散磁共振成像在急性缺血性脑卒中的应用   总被引:7,自引:3,他引:4  
目的 评估磁共振 (MRI)弥散加权成像 (DWI)及灌注加权成像 (PWI)在急性缺血性卒中指导溶栓治疗的应用价值。方法 对 44例急性 (≤ 6h)缺血性卒中患者行DWI、PWI扫描 ,DWI及PWI的不匹配区为缺血半暗带 ,根据半暗带是否存在确定患者是否适合溶栓治疗。结果 脑梗死患者 33例 ,其中 2 3例 (52 3 % )有明显半暗带存在 (PWI >DWI) ;1 0例 (2 2 7% )无明显半暗带 (PWI=DWI)。临床表现为短暂性缺血发作 (TIA)者 1 1例 (2 5 0 % )。结论 PWI及DWI对照研究有助于发现超早期脑梗死半暗带 ,指导溶栓治疗 ;临床表现结合DWI有助于除外TIA  相似文献   

10.
海风藤提取物对脑缺血保护作用的实验研究   总被引:4,自引:0,他引:4  
目的:探讨血小板活化因子(PAF)受体拮抗剂海风藤提取物对鼠脑缺血半暗带神经细胞凋亡的影响,并与传统的PAF受体拮抗剂银杏苦内酯相比较。方法:采用流式细胞分析和TUNEL方法,观察各实验组鼠脑缺血半暗带神经细胞的凋亡,并结合电镜观察缺血神经细胞超微结构的改变。结果:假手术组仅有极少量神经细胞凋亡;缺血90min再灌注12、24h缺血半暗带神经细胞凋亡明显增多;海风藤提取物、银杏苦内酯治疗组于相同时限内细胞凋亡较缺血/再灌组显著减少。结论:海风藤提取物与传统PAF受体拮抗剂银杏苦内酯均能明显减少缺血半暗带神经细胞的凋亡数量,减缓缺血区神经元损害,具有显著的脑保护作用。  相似文献   

11.
The growth and progression of traumatic brain injury (TBI) lesions depend significantly on developments in the traumatic penumbra area, perilesional region, where delayed neuronal death occurs. Recent data supports the important role of apoptosis in delayed cell death in TBI. Previously we demonstrated a significant reduction of apoptosis in traumatic penumbra in animals treated by hyperbaric oxygen (HBO).In this study we evaluate the expression of apoptosis-related proteins of the Bcl-2 family (Bcl-2, Bax and Bcl-xL) in the traumatic penumbra area in correlation with the extent of apoptosis in the rat model of focal cerebral contusion, treated by HBO. Sprague-Dawley rats underwent cortical dynamic deformation, some with subsequent hypoxemia. A group of both hypoxemic and non-hypoxemic animals was treated by HBO. The pathological study was based on immunohistochemical staining of the brain sections for Bcl-2, Bax and Bcl-xL with quantitative evaluation of staining by image analysis. The expression of Bcl-2 in hypoxemic animals was lower than in non-hypoxemic animals, but a significant increase in Bcl-2 expression was seen in both groups after HBO treatment. Bcl-xL also demonstrated an increase after HBO treatment but less significant. Staining for Bax protein did not demonstrate significant change after treatment. These data correlate well with the reduction of TUNEL-positive cells in traumatic penumbra after HBO treatment. We concluded that the apoptotic mechanisms are important in delayed cell death in TBI and that post-traumatic hypoxemia increases the intensity of apoptosis, probably through a decrease in Bcl-2 and Bcl-xL expression which normally repress apoptosis. The beneficial effect of HBO treatment in our model of brain contusion correlates well with the increased expression of anti-apoptotic proteins (Bcl-2 and Bcl-xL) following treatment and the appropriate decrease in the extent of apoptosis. In light of these results, the usage of HBO is justified as neuroprotective treament in TBI.  相似文献   

12.
目的观察针灸即时和治疗后对脑挫裂伤局部血流变化影响结果,以确定缺血半暗区(IP)的存在和针灸疗效。方法将60例脑挫裂伤患者随机分成2组,针灸组30例,在常规治疗基础上加用针刺疗法;对照组30例采用常规治疗。通过ECT脑显像分别进行针灸组针刺前后及治疗14d后、对照组治疗前后及治疗14d后的局部脑血流量(rCBF)对比观察。结果脑挫裂伤损伤部位存在血流量减低的IP,针灸组首次针灸前后rCBF比较有极显著差异(P<0.001),治疗14d后其变化差异亦极显著(P<0.001)。对照组治疗前后rCBF比较差异极显著(P<0.001),两组治疗后rCBF比较差异亦极显著(P<0.005)。结论脑显像可直观的反映脑挫裂伤病人损伤区局部脑血流变化,提示脑挫伤区存在着IP,针刺治疗能明显改善局部脑血流量,为针刺治疗脑挫裂伤提供了依据。  相似文献   

13.
Cerebral contusions are one of the principal lesions of traumatic brain injury and the attendant oedema formation contributes substantially to the clinicopathological manifestations. While it is now recognised that the membrane channel protein aquaporin-4 (AQP-4) plays a major role in the development and resolution of cerebral oedema, assessments of its expression in and around contusions have produced conflicting results. We used an ovine impact-acceleration model of closed head injury to examine contusion-related AQP-4 expression and found that there was a heterogeneous AQP-4 response within contusions, with some astrocytes being nonviable and immunonegative, while others showed increased AQP-4 expression. Pericontusional astrocytes in the penumbra region generally showed more robust AQP-4 immunopositivity than intracontusional glia. Thus, manipulation of AQP-4 expression could have therapeutic applications in controlling cerebral oedema associated with contusions.  相似文献   

14.
bFGF、VEGF在大鼠创伤脑组织中的表达   总被引:13,自引:2,他引:11  
目的研究碱性成纤维细胞生长因子(bFGF)和血管内皮生长因子(VEGF)在大鼠创伤脑组织中的表达及它们之间的关系,从分子水平探讨颅脑损伤后的病理机制,为临床治疗脑损伤的新途径提供实验基础。方法 改进Marmarou大鼠加速弥漫性脑损伤模型,制作成弥漫性轴索损伤同时合并局灶性脑挫伤的新的动物模型,取挫伤灶周围脑组织免疫组化染色观察bFGF、VEGF基因表达情况。结果 脑挫伤灶周围脑组织bFGF基因表达在伤后1h明显增加,伤后12h达高峰;VEGF基因表达伤后逐渐增加,24h达高峰。结论 bFGF、VEGF基因表达与脑损伤密切相关,bFGF、VEGF作为生长因子可能参与颅脑损伤后神经元保护及损伤后修复过程。  相似文献   

15.
高血压脑出血半暗带早期病理变化及脑保护的实验研究   总被引:2,自引:0,他引:2  
目的研究高血压脑出血后血肿周半暗带的病理变化及早期保护措施。方法通过立体定向手术脑尾状核胶原酶加肝素联合注射诱导大鼠出血模型,采用30只卒中倾向的自发性高血压大鼠(SHRSP),体重200~230 g,随机分为2组,观察组和携氧液组。治疗组于血肿形成早期给予携氧液治疗,观察血肿周组织形态及超微结构。结果出血后6小时,观察组血肿周边神经细胞就普遍变性,大量脱髓鞘变化,并有凋亡小体形成。携氧液组患侧组织形态学及细胞超微结构改变明显减轻。结论高血压脑出血后血肿周边半暗带早期就产生显著的病理改变,携氧液对高血压的血肿周脑组织有良好的保护作用。  相似文献   

16.
急性局灶性脑缺血后细胞凋亡的动态变化   总被引:4,自引:0,他引:4  
目的:细胞凋亡是细胞死亡的一种形式,对缺血后梗塞灶的发生,发展一定的作用。故测定缺血脑区出现DNA片断化的细胞数量变化及在缺血脑区的分布状况,以了解脑缺血的病理生理及寻求防治措施。方法:利用线栓法制成大脑中动脉缺血动物模型,测定脑组织SOD,LPO含量变化及凋亡细胞的密度变化;  相似文献   

17.
目的:探讨CT对外伤性迟发性脑挫裂伤的诊断价值。方法回顾分析我院收集的85例外伤性迟发性脑挫裂伤患者的CT检查结果,主要分析迟发性脑挫裂伤CT检查时间、检查部位以及大小等。结果外伤性迟发性脑挫裂伤的CT检查的最佳时间通常在伤后24h后,一般情况下血肿并不大,脑外围额叶为多发部位。结论CT检查诊断外伤性迟发脑挫裂伤最佳检查时间在伤后48~72h内,临床主要用于外伤性迟发性脑挫裂伤的症状持续存在或加重情况下的及时复查。  相似文献   

18.
《中国神经再生研究》2016,(8):1260-1266
Neuronal apoptosis is mediated by intrinsic and extrinsic signaling pathways such as the membrane-mediated, mitochondrial, and endo-plasmic reticulum stress pathways. Few studies have examined the endoplasmic reticulum-mediated apoptosis pathway in the penumbra after traumatic brain injury, and it remains unclear whether endoplasmic reticulum stress can activate the caspase-12-dependent apoptotic pathway in the traumatic penumbra. Here, we established rat models of lfuid percussion-induced traumatic brain injury and found that protein expression of caspase-12, caspase-3 and the endoplasmic reticulum stress marker 78 kDa glucose-regulated protein increased in the traumatic penumbra 6 hours after injury and peaked at 24 hours. Furthermore, numbers of terminal deoxynucleotidyl transferase-mediat-ed dUTP nick end labeling-positive cells in the traumatic penumbra also reached peak levels 24 hours after injury. These ifndings suggest that caspase-12-mediated endoplasmic reticulum-related apoptosis is activated in the traumatic penumbra, and may play an important role in the pathophysiology of secondary brain injury.  相似文献   

19.
Topography of c-fos immunoreactivity in an ovine head impact model.   总被引:1,自引:0,他引:1  
Cortical neuronal and glial c-fos immunoreactivity has been demonstrated in experimental and human brain injury. c-fos is one of the immediate early genes important in signal transduction linking environmental stimuli to the cellular genome. c-fos immunoreactivity was semi-quantitated in a head impact sheep model using a grid system applied to standard coronal brain sections obtained from 12 impacted and 4 control sheep. Substantial glial and neuronal c-fos immunoreactivity was present in the pericontusional (penumbra) region, but was absent or minimal in the core of the contusion. Apart from these focal changes, c-fos immunoreactivity was diffusely distributed, with greater involvement in the cerebrum on the side of impact. In the cerebellum, Bergmann glia showed prominent c-fos immunoreactivity, while Purkinje cells were consistently immunonegative. c-fos immunoreactivity varied in different regions of the brain (focal and diffuse patterns) in this ovine head impact model.  相似文献   

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