高血压在局部脑梗塞边缘区和镜区脑超微结构的动态改变中的意义

本文实验发现双肾双夹肾血管性高血压大鼠（RHR）在大脑中动脉闭塞（MCAO）后1-7天，梗塞灶边缘区有脑微血栓形成，MCAO后3天对侧半球的相应区（镜区）有较明显的微血管变形和星形细胞足突水肿改变，说明RHR与正常的SD鼠在局灶脑梗塞后的超微结构改变是不同的。因此，我们应当重视高血压的防治。     

肾血管性高血压大鼠的大脑表面侧支吻合血管改变

高血压脑动脉硬化是脑梗塞的主要危险因素之一。我们已复制了可靠而稳定的肾血管性高血压大鼠(RHR)模型,并观察到RHR脑血管的形态结构改变。本研究用脑血管铸型方法,实验比较RHR与正常血压大鼠的脑表面侧支吻合血管情况,旨在探     

急性脑损伤脑微血管三维构型和超微结构实验研究

通过血管铸型方法观察急性脑损伤动物模型脑微血管三维结构和血管内皮细胞的超微结构改变。结果发现：脑损伤后，脑微血管内皮细胞发生显著变性，脑微血管痉挛，小动脉、毛细血管断裂以及出现多处无毛细血管区。本实验证实，脑损伤以后，发生明显的脑微血管系统出血性和缺血性改变，病灶区血液循环障碍。这些发现有力地支持继发性脑损害血管源性机制的假说。     

高血压在局部脑梗塞边缘区和镜区脑超微结构的动态改变中的意义

本文实验发现双肾双夹肾血管性高血压大鼠（ＲＨＲ）在大脑中动脉闭塞（ＭＣＡＯ）后１～７天，梗塞灶边缘区有脑微血栓形成，ＭＣＡＯ后３天对侧半球的相应区（镜区）有较明显的微血管变形和星形细胞足突水肿改变，说明ＲＨＲ与正常的ＳＤ鼠在局灶脑梗塞后的超微结构改变是不同的。因此，我们应当重视高血压的防治。     

脑活素抗局灶脑缺血再灌流损伤的实验研究

目的观察脑活素对局部脑缺血再灌流损伤的保护作用。方法以易卒中型肾血管性高血压大鼠复制可再灌流的ＭＣＡＯ模型，用光镜、电镜及图像分析比较了脑活素和对照组的脑梗死灶及脑微血管超微结构改变。结果脑活素组大鼠死亡数下降，并发脑出血例数减少。再灌流７～１４天，脑梗死灶面积较对照组的小，脑微血管损害减轻。结论脑活素可减轻局灶脑缺血再灌流后脑水肿，缩小梗死灶，对脑微血管损伤有一定保护作用     

降纤酶对实验性脑梗死灶周围微血管作用的观察

目的研究降纤酶对实验性脑梗死灶周围微血管的作用。方法用线栓法将易卒中型肾血管性高血压大鼠(stroke-pronerenovascularhypertensiverats,RHRSP)复制成一侧大脑中动脉闭塞(MCAO)模型,静脉注射降纤酶,对照组注射生理盐水,分别于缺血3、6、24h进行功能评分并处死大鼠,TTC染色计算脑梗死范围,HE染色观察梗死边缘区的病理形态,同时免疫组织化学检测尿激酶型纤溶酶原激活剂(urokinasetypeplasminogenactivator,uPA)和纤溶酶原激活剂抑制物1(plasminogenactivatorinhibitor1,PAI1)蛋白的表达。结果降纤酶能改善MCAO后神经功能评分,减少梗死灶体积,梗死灶边缘微血管损害减轻,血管内皮uPA蛋白表达减少及PAI1蛋白表达增加。结论降纤酶可能是通过抑制微血管内皮细胞uPA蛋白表达和增加PAI1蛋白表达而减轻脑梗死灶边缘微血管损害。     

西比灵对大鼠高血压性脑血管病变作用的研究

目的 探讨西比灵对大鼠高血压性脑血管病变的作用及其机制。方法 建立肾血管性高血压大鼠（RHR）模型。用插胃管法喟食西比灵对RHR进行治疗，观察动脉血压，脑血流速度和脑血管形态的改变。结果 用药2-4周动脉血压明显低于同期未用药RHR，4-6周后脑底动脉内腔面积，横断面积，中膜厚度等明显好于未用药RHR，这些作用可以持续2-4周。结论 在高血压早期，西比灵可以降低RHR的动脉血压，阻止脑血管损害的发展。     

局部脑梗塞再灌流边缘区血脑屏障超微结构改变

目的观察局部脑梗塞再灌流边缘区血脑屏障（ＢＢＢ）超微结构的动态变化。方法用改良的Ｌｏｎｇａ氏方法，在肾血管性高血压大鼠获得可靠的大脑中动脉闭塞及再灌流模型，观察梗塞灶边缘区超微结构改变。结果局部脑梗塞早期恢复血流对病灶边缘区并没有加重ＢＢＢ损害，多形核白细胞阻塞毛细血管也是加重微循环障碍和ＢＢＢ损害的因素。结论必须重视ＢＢＢ损害在脑梗塞时的重要作用，注意对ＢＢＢ损害的防治，早期主要是恢复供血，提示溶栓可能有益     

易卒中型肾血管性高血压大鼠脑微血管超微结构观察

动态观察了易卒中型肾血管性高血压大鼠在高血压不同时期和卒中急性期的脑微血管病变。发现高血压早期已有脑微血管损害,并随血压升高和持续时间延长而加重,至高血压晚期出现管腔狭窄,内皮细胞水肿。此时虽未发生卒中,但受损微血管周围的神经细胞已出现线粒体肿胀,内质网扩张等缺血缺氧表现。卒中时,管壁结构严重破坏,有的管腔闭塞。显示高血压时脑微血管病变在高血压动脉硬化性卒中发病中起重要作用。     

局灶性脑梗塞和再灌注后边缘区血脑屏障超微结构的改变

局灶性脑梗塞和再灌注后边缘区血脑屏障超微结构的改变李玲，黄如训，苏镇培一、资料与方法肾性高血压大鼠（ＲＨＲ）采用改良的Ｌｏｎｇａ氏颈动脉放线，闭塞大脑中动脉（ＭＣＡＯ）造成局灶性脑梗塞和再灌注模型。应用透射电镜动态观察ＲＨＲ脑梗塞和再灌注后梗塞灶边缘...     

肾血管性高血压大鼠脑梗塞后脑微血管形态计量学动态观察

本研究选用双肾双夹肾动脉狭窄术复制成的肾血管性高血压大鼠（ＲＨＲ）５４只；同龄正常血压鼠（ＳＤＲ）５４只，各分为大脑中动脉闭塞（ＭＣＡｏ）前、后不同时间的９个实验和对照组，各组均即时从心腔等压灌注中华墨汁，取脑顶叶梗塞灶边缘区，行冠状、矢状、水平三方向取材，制片，在显微镜下作微血管形态计量学测定．结果显示ＲＨＲ顶叶脑皮质毛细血管直径、单位体积毛细血管长度、表面积、通过２００μｍ的毛细血管支数均较ＳＤＲ减少，表明高血压可致脑微血管稀疏；同时观察到局部脑梗塞后上述反映毛细血管网三维构筑的参数变化远较对照鼠明显，缺血后脑损伤更严重。说明毛细血管损伤程度与梗塞灶的大小直接相关，因此应加强高血压的防治，以保护脑微血管立体构筑。     

Assessment of postischemic cerebral energy metabolism in cat by 31P NMR: the cumulative effects of secondary hypoxia and ischemia

The sensitivity of cerebral energy metabolism to ischemic and hypoxic stresses following global cerebral ischemia was evaluated in a cat model using 31P nuclear magnetic resonance (NMR) spectroscopic methods. Complete global cerebral ischemia of 5 to 10 min in length was produced at 1 h intervals by reversible arterial occlusion, permitting continuous monitoring of NMR and EEG. Ischemia appeared to produce slightly more severe energy failure in animals that had previously experienced an ischemic injury. Preischemic hypoxia (5% O2 for 5 min) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate, which were slightly amplified in animals that previously experienced ischemia.     

Selective cortical neuronal damage after middle cerebral artery occlusion in rats

We studied histopathologic changes in cerebral cortex of 20 rats after middle cerebral artery occlusion by using the Fink-Heimer suppressive silver impregnation method and conventional stains. At 6 hours after occlusion, Fink-Heimer-stained sections revealed abundant coarsely granular, intensely argyrophilic neurons in the ischemic cortex. These distinctive argyrophilic neurons could be clearly differentiated from neurons that suffered postmortem changes; argyrophilic neurons were present in all layers of the lateral parietal cortex but in only the superficial cortical layers II and III in the parasagittal area of the frontoparietal cortex and the temporo-occipital area. At 24 hours after occlusion as the ischemic region progressed to pannecrosis, argyrophilic neurons were still evident in peri-infarct regions, with more prominent neuritic silver deposits but no changes in number or spatial distribution. Over 2-7 days, the argyrophilic neurons gradually disappeared while many fine silver-impregnated degenerating terminals appeared in the peri-infarct regions. At 3-6 weeks after occlusion, no more argyrophilic neurons were seen in the cortex although degenerating axons were still present in the deep white matter. Our results indicate selective neuronal damage in the superficial cortical layers and massive axonal degeneration in the cerebrum surrounding infarcts. The neuronal damage does not appear to progress beyond 6 hours after middle cerebral artery occlusion. The Fink-Heimer method has many advantages over existing conventional stains for documenting selective neuronal damage in focal cerebral ischemia.     

脑缺血再灌流脑微血管损害及u-PA表达的实验研究

目的探讨脑缺血再灌流后继发的脑水肿、出血的发生机制。方法应用光镜、透射电镜、免疫组织化学、显微镜－计算机图像分析等技术，观察大鼠局部脑缺血２小时再灌流不同时间，脑微血管结构、Ⅳ型胶原抗原及尿激酶型纤溶酶原激活物（ｕ－ＰＡ）表达。结果局部脑缺血再灌流２４小时，缺血侧ＭＣＡ区脑微血管外细胞间质水肿最严重，基底膜节段性溶解、缺损，有红细胞漏出，微血管壁及管外细胞间质ｕ－ＰＡ大量表达达高峰，同时微血管基底膜Ⅳ型胶原抗原减少。随再灌流时间延长，微血管基底膜损害加重，Ⅳ型胶原抗原逐渐消失，ｕ－ＰＡ表达减少。结论脑缺血再灌流后脑微血管结构损害是导致脑水肿、出血的主要病理基础，而脑微血管壁和管外细胞间质ｕ－ＰＡ表达可能是引起微血管损害的主要机制之一。     

Antileukocyte therapy of cerebral ischemic stroke in MCAO model in rats

OBJECTIVE To Study protecting effect of antileukocytic drugs on cerebrol ischemic injury. BACKGROUND The purposes of prcsent study aimed at comparing the protecting effect of some antileukocytic drugs: chloroquine, Colchieine, Cyclophosphamid (CTX) ,Cyclosporin A, Multiglycoside tripteygil against cerebral ischemic injury in MCAO models in the rats. METHODS 130 SD rats with MCAO model randomly divided into one control group and 10 treatment groups. The observation items were as follows: (1) The infarction volume. (2) Brain edema. (3) Histopathoiogical evaluation. (4) The count of neurons and microglia cells in the infarction area. (5) Neurological dysfunction score. (6) The determination of serum lL-1 β and TNF- α levels. RESULTS Antileukocytic drugs can decrease the volume of infarction, brain edema, inflammatory reaction and neuron death of ischemic injury, the low dose of chloroquine plus colchicine plus CTX had better effects, and prolonged therapeutic time windows. DISCUSSION The accumulation of infiammatory cell and cytoking release from them can promote and increase neuron death in infarction area. CONCLUSION Antileukocytic drugs are of protecting effect on ischemic neuron in MCAO model in rats.     

脑缺血再灌注损伤后GAP-43蛋白的表达和意义

目的 探讨脑缺血再灌注损伤后生长相关蛋白-43（GAP-43）的表达对神经元轴突再生的可塑性变化.方法 成年健康雄性Wistar大鼠40只,随机分为正常对照组、假手术组和缺血1h再灌注2h、6h、12h、24h、48h、3d、7d、14d组,每组各4只（n=4）.应用线栓法制备大鼠脑中动脉闭塞再灌注模型（MCAO）,采用免疫组织化学方法检测GAP-43的表达并观察神经元轴突再生的变化,并进行计算机图像分析.结果 缺血再灌注2h,海马、皮质区及纹状体区GAP-43呈基础表达,6h、12h、24h、48h表达逐渐增高,7d达高峰,P＜0.05,14d达最低表达,P＜0.05.与假手术组比较有显著性差异,P＜0.05.正常对照组无表达.缺血再灌注48h～7d损伤区域神经元轴突呈出芽征,发出突触纤维.结论 脑缺血再灌注损伤后GAP-43呈非特异性表达,并促进神经元的修复和再生.     

The developing profile of cerebral ischemia

Cerebral ischemia, which may be silently manifested as transitory ischemia attacks or cerebral infarction, is not a stable, but rather, a moving process. In cerebral infarctions the initial ischemic area may change or move in a high percentage of patients and may involve a significant volume (mean of 32%) of neuronal tissue. The negative changes of initial cerebral ischemia which produce a worsening of the same may be due to the progression of the thrombus, appearance of new embolisms, cerebral edema, hemorrhage, blood reperfusion and systemias causes. These changes may determine the conversion of the shaded ischemic area into a definitive, irreversible infarction. The negative changes may also be produced some distance from the initial ischemic area, either because of microthromboembolisms or diaschisis. The positive changes of initial cerebral ischemia which produce as improvement of the same, may be due to collateral circulation, lysis or fragmentation of the embolism and a decrease in cerebral edema. Clinical changes with no evident clinical manifestations may also be produced and may be diagnosed with the use of clinical scales, imaging techniques, ultrasound and hematological and biochemical markers. Acknowledgement of these cerebral ischemia changes in the acute phase may determine the salvation of a part of the brain, and thereby modify the future clinical situation of the patient.     

Changes in tissue factor and the effects of tissue factor pathway inhibitor on transient focal cerebral ischemia in rats

INTRODUCTION: To determine the contribution of tissue factor (TF) to focal cerebral ischemia/reperfusion injury, we investigated the changes in TF in rat brains with transient focal cerebral ischemia and also assessed the effect of TF pathway inhibitor (TFPI). MATERIALS AND METHODS: Spontaneous hypertensive rats were subjected to 90-min of middle cerebral artery occlusion (MCAO) and then were reperfused for up to 24 h. Immediately after MCAO, recombinant human TFPI (rhTFPI) (50 or 20 microg/kg/min) was administered by means of a continuous intravenous injection for 4.5 h. RESULTS AND CONCLUSIONS: TF immunoreactivity decreased or scattered in the ischemic area after reperfusion, however, an increased TF expression was observed in the microvasculature with the surrounding brain parenchyma and it peaked at 3 to 6 h, which coincided with the start of fibrin formation. On the other hand, total TF protein in ischemic area continued to exist and did not remarkably change until 24 h after reperfusion. At 24 h after reperfusion, the total infarct volume in the group treated with 50 microg/kg/min rhTFPI was significantly smaller than that in the controls (saline). Western blotting and immunohistochemical studies showed that rhTFPI treatment resulted in a decrease of fibrin in the ischemic brains and microvasculature. TF-mediated microvascular thrombosis is thus considered to contribute to focal cerebral ischemia/reperfusion injury. The continuous infusion of rhTFPI until a peak of TF-mediated microvascular thrombosis therefore attenuates the infarct volume by reducing fibrin deposition in the cerebral microcirculation.     

大鼠脑缺血再灌注损伤后脑组织STAT3变化的免疫组织化学研究

目的 探讨信号转导和转录激活子（ＳＴＡＴ）３在大鼠局灶性脑缺血再灌注损伤中的表达及其与缺血性神经细胞损伤的关系方法 用ＡＢＣ免疫组化方法观察大鼠局灶性脑缺血再灌注损伤后脑组织中的ＳＴＡＴ３蛋白免疫反应阳性细胞分布。结果 正常和假手术大鼠脑内以及脑缺血后的非缺血半球脑组织中未发现有ＳＴＡＴ３免疫反应阳性细胞,脑缺血再灌注损伤后１２小时在栓塞侧梗死区可见少量ＳＴＡＴ３免疫阳性细胞,２４小时后阳性细胞显著增多达高峰,在缺血侧纹状体和缺血皮质周边区表达最明显,１周后梗死周边区少数神经细胞仍有阳性表达。差异有显著意义（Ｐ〈０．０１）。结论 ＳＴＡＴ３活化及超量表达可能介导了缺血神经细胞信号转导过程,并参与了脑缺血神经细胞损伤与修复的病理生理过程。     

Rodent models of cerebral ischemia

The use of physiologically regulated, reproducible animal models is crucial to the study of ischemic brain injury--both the mechanisms governing its occurrence and potential therapeutic strategies. Several laboratory rodent species (notably rats and gerbils), which are readily available at relatively low cost, are highly suitable for the investigation of cerebral ischemia and have been widely employed for this purpose. We critically examine and summarize several rodent models of transient global ischemia, resulting in selective neuronal injury within vulnerable brain regions, and focal ischemia, typically giving rise to localized brain infarction. We explore the utility of individual models and emphasize the necessity for meticulous experimental control of those variables that modulate the severity of ischemic brain injury.