山楂总黄酮注射液对大鼠大脑中动脉血栓所致局部脑缺血性损伤的保护作用

目的观察山楂总黄酮注射液对大鼠大脑中动脉血栓所致局部脑缺血性损伤的保护作用。方法采用三氯化铁局部涂抹损伤血管形成大鼠大脑中动脉血栓模型,以脑梗死范围、脑含水量为观察指标,研究山楂总黄酮对大脑中动脉血栓所致局部脑缺血的预防作用。结果山楂总黄酮12mg/kg、24mg/kg、48mg/kg静脉注射均可显著降低大鼠局灶性脑缺血损伤后脑含水量,山楂总黄酮24mg/kg及48mg/kg静脉注射可显著降低大鼠脑梗死范围。结论山楂总黄酮注射液对脑缺血性损伤具有良好的保护作用。     

罗布麻提取物对大鼠局灶性脑缺血再灌注损伤的保护作用

目的 观察罗布麻提取物（Aplocyilum venetum L Extract,AVE）对大鼠局灶性脑缺血再灌注损伤的保护作用。方法 将雄性Wistar大鼠随机分为假手术组、模型组、AVE（高、低剂量）组和阳性对照组（银杏叶胶囊）,口服给药5d后,采用改良的Ionga法,建立大鼠局灶性脑缺血再灌注损伤模型。再灌注2,4h后对大鼠神经功能障碍进行评分,测量其脑梗死面积、脑含水量。结果 与模型组相比,AVE两个剂量组可以减轻神经症状,缩小缺血面积,并且可以减轻脑水肿。与阳性对照组对比,各指标无显著性差异。结论 AVE对局灶性脑缺血再灌注模型大鼠具有保护作用。     

高压氧对大鼠急性局灶性脑缺血再灌注损伤血管通透性的影响(论著)

目的：探讨高压氧（ＨＢＯ）对大鼠急性局灶性脑缺血再灌注损伤血管通透性的影响。方法：应用血管内细丝栓堵脑中动脉（ＭＣＡ）的局灶性脑缺血大鼠模型。利用免疫组织化学方法，观察ＭＣＡ缺血１小时，再灌注４、１１、２３、７１小时脑血管通透性的变化，在以上期间同时应用常压纯氧和常规临床治疗压力０．２５ＭＰａＨＢＯ于开始缺血后２、９、２１、４５和６９小时分别治疗１次（１小时）。结果：常压纯氧组与缺血再灌注（ＩＲ）组相比脑水肿面积无明显差异，而ＨＢＯ组和ＩＲ组相比脑水肿面积分别缩小了１２．２８％（视交叉前平面），２０．４７％（视交叉平面）和８．５１％（视交叉后平面），两组间存在非常显著性差异（Ｐ＜０．０１）。结论：ＨＢＯ可明显抑制大鼠急性局灶性脑缺血再灌注损伤血管通透性的增加。     

甾体皂苷化合物抑制血栓形成作用的研究

目的：观察甾体皂苷化合物(化合物9714)对血栓形成、血小板聚集及血液流变学的影响。方法：采用动静脉旁路血栓形成模型，测定化合物9714对血栓形成的影响；采用比浊法，测定其对大鼠血小板聚集的影响；采用大鼠急性血淤模型，测定其对血液流变学的影响。结果：化合物971410，20，40mg／kg组均能明显减轻血栓的干重及湿重；可抑制ADP、胶原诱导的大鼠血小板聚集；降低急性血淤大鼠的全血黏度、血浆黏度、红细胞聚集性，以及增强红细胞变形性。结论：化合物9714通过抑制血小板聚集、改善血液流变学来发挥其抗血栓形成作用。     

线栓法所致大鼠局灶性脑缺血/再灌注后脑水肿的时程变化

目的：研究线栓法所致大鼠局灶性脑缺血／再灌注后脑水肿的时程变化。方法：用线栓法，制造大鼠大脑中动脉阻塞的脑缺血／再灌注动物模型，采用干湿称重法测定脑缺血／再灌注后，不同时刻大鼠损伤侧脑组织的含水量。结果：脑缺血3h，大鼠损伤侧脑组织含水量开始增高，随着再灌注的进行，脑组织含水量继续缓慢增高，至再灌注4h时显升高，直至再灌注16h时达到最高。结论：线栓法所致大鼠局灶性脑缺血／再灌注后，脑水肿的程度在16h内呈进行性加重。     

地塞米松抑制白细胞功能可防治大鼠脑缺血性损伤

凝闭大鼠一侧大脑中动脉，造成局灶性脑梗塞后２４小时，大鼠外周中性粒细胞活性增强；缺血区脑组织脂质过氧化损伤严重；ＴＴＣ染色后可见边界明显的脑坏死区。地塞未松可抑制脑缺血所致的中性粒细胞吞噬化学发光增强，减少白细胞在缺血区的浸润，减轻组织脂质过氧化损伤，保护ＳＯＤ活性，缩小梗塞范围。其抑制粒细胞功能激活与减轻脑缺血性损伤之间有显著的正相关关系。提示：脑梗塞时，激活的外周白细胞能加重脑缺血性损伤；地塞米松抑制白细胞功能的作用可能是其防治脑梗塞的机制之一。     

WIN55，212-2对大鼠局灶性脑缺血再灌注损伤的保护作用

目的：探讨大麻素（CB）受体激动剂WIN55，212-2对大鼠局灶性脑缺血的保护作用。方法：采用大鼠大脑中动脉栓塞（MCAO）致局灶性脑缺血模型。将50只雄性SD大鼠随机分为5组：对照组（Con组）于MCAO前30min腹腔注射生理盐水0．3ml；WIN55，212-2组（WIN1～3组）于MCAO前30min腹腔注射WIN55，212-20．3，1和3mg／kg；DMSO组于MCAO前30min腹腔注射二甲基亚砜（DMSO）0．3ml。观察MCAO120 min再灌注24h后神经功能评分（NFS）和脑梗死容积百分比。结果：与DMSO组和Con组比较，WIN55，212-2组大鼠NFS明显升高（P〈0．05），脑梗死容积百分比明显减小（P〈0．05）。结论：CB受体激动剂WIN55，212-2对大鼠局灶性脑缺血再灌注损伤具有保护作用，并具有一定的剂量相关性。     

参丹脑梗通注射液抗大鼠急性脑梗死损伤作用的研究

目的研究三药配伍复方注射液参丹脑梗通注射液的抗大鼠急性脑梗死损伤作用。方法建立冷光源光化学诱导大鼠大脑中动脉脑血栓形成模型。SD大鼠按体质量随机分为假手术组、模型组、参丹脑梗通注射液高、中、低剂量组(19.6、9.8、4.9 mg·kg-1)和盐酸川芎嗪注射液组(19.6 mg·kg-1),观察受试物对脑缺血大鼠神经功能缺失症状、脑含水量、脑梗死灶面积、脑组织MDA含量,SOD、GSH-Px和LDH活性的影响。结果参丹脑梗通注射液能够显著改善局灶性脑缺血大鼠神经功能障碍,减少脑梗死灶面积和MDA含量,增加SOD、GSH-Px和LDH活性,并且在相同剂量下(19.6 mg·kg-1),上述效果均优于盐酸川芎嗪注射液。结论三药配伍复方注射液参丹脑梗通注射液具有较好的抗局灶性脑缺血作用,其效果优于临床上的单方制剂。     

脑缺血再灌注的炎症损伤分子机制及吲哚美辛的保护作用

目的 研究大鼠局灶性脑缺血再灌注炎症损伤的分子机制,并观察吲哚美辛对脑缺血再灌注炎症损伤的保护作用.方法 36只雄性SD大鼠随机分为假手术组,模型组,吲哚美辛3、6、9mg/kg组,每组6～8只.应用线栓法制作大鼠局灶性脑缺血再灌注模型,缺血2h再灌注24h后处死动物,以TTC染色法测定脑梗死范围和神经功能缺损情况,并分别采用ELISA、Western blot法检测脑组织中IL-8、IL-1β、TNF-α、髓过氧化物酶(MPO)含量以及细胞间黏附分子1(ICAM-1)、E选择素(E-selectin)的表达.结果 吲哚美辛能明显减小模型大鼠的脑梗死范围,减轻神经损伤症状;预先给予吲哚美辛(6、9mg/kg)可降低脑组织中MPO活性及IL-8、IL-1β、TNF-α的水平,并减少ICAM-1、E-selectin的表达(P＜0.05或0.01).结论 吲哚美辛可通过抑制脑缺血再灌注过程中炎症介质的表达和释放,降低脑缺血再灌注所致的炎症损伤.     

地塞米松抑制白细胞功能防治大鼠脑缺血性损伤研究

凝闭大鼠一侧大脑中动脉,造成局灶性脑梗塞24h后,大鼠外周中性粒细胞活性增强;缺血区脑组织脂质过氧化损伤严重;TTC染色后可见边界明显的脑坏死区。地塞米松可抑制脑缺血所致的中性粒细胞吞噬化学发光增强,减少白细胞在缺血区的浸润,减轻组织脂质过氧化损伤,保护SOD活性,缩小梗塞范围。其抑制粒细胞功能激活与减轻脑缺血性损伤之间有显著的正相关关系。提示:脑梗塞时,激活的外周白细胞能加重脑缺血性损伤;地塞米松抑制白细胞功能的作用可能是其防治脑梗塞的机制之一。     

WIN 55,22-2对大鼠局灶性脑缺血再灌注损伤的保护作用

目的:探讨大麻素(CB)受体激动剂WIN55,212-2对大鼠局灶性脑缺血的保护作用。方法:采用大鼠大脑中动脉栓塞(MCAO)致局灶性脑缺血模型。将50只雄性SD大鼠随机分为5组:对照组(Con组)于MCAO前30 min腹腔注射生理盐水0.3 ml;WIN55,212-2组(WIN1~3组)于MCAO前30 min腹腔注射WIN55,212-2 0.3,1和3 mg/kg;DMSO组于MCAO前30 min腹腔注射二甲基亚砜(DMSO)0.3 ml。观察MCAO120 min再灌注24 h后神经功能评分(NFS)和脑梗死容积百分比。结果:与DMSO组和Con组比较,WIN55,212-2组大鼠NFS明显升高(P<0.05),脑梗死容积百分比明显减小(P<0.05)。结论:CB受体激动剂WIN55,212-2对大鼠局灶性脑缺血再灌注损伤具有保护作用,并具有一定的剂量相关性。     

Effects of blood sugar level on rat transient focal brain ischemia consecutively observed by diffusion-weighted EPI and (1)H echo planar spectroscopic imaging.

The effects of blood sugar level on transient focal brain ischemia were examined by consecutive diffusion-weighted EPI and (1)H echo planar spectroscopic imaging. A remote-controlled rat intraluminal suture middle cerebral artery occlusion (MCAO) model was prepared. Animals were divided into three experimental groups: control, 1 g/kg, and 2 g/kg glucose groups (n = 6 for each). Saline or glucose was infused intraperitoneally 30 min prior to MCAO. The glucose-loaded groups showed increased lactate accumulation and marked decreases in average diffusion coefficient in the ischemic region during 40-min MCAO. These changes were correlated with blood sugar levels at the onset of MCAO. After reperfusion, all rats in the control and 1 g/kg groups recovered from the ischemic changes, but three rats with marked hyperglycemia in the 2 g/kg group showed irreversible changes. The adverse effects of hyperglycemia on transient focal brain ischemia were clearly demonstrated by sequential 2D images. Magn Reson Med 42:895-902, 1999.     

Microplasmin and tissue plasminogen activator: comparison of therapeutic effects in rat stroke model at multiparametric MR imaging

PURPOSE: To prospectively compare therapeutic and hemorrhagic effects of microplasmin and tissue plasminogen activator (tPA) in stroke therapy by using multiparametric magnetic resonance (MR) imaging in a photothrombotic rat stroke model. MATERIALS AND METHODS: The animal experiment complied with institutional regulations for laboratory animals. Stroke was induced in rats with photothrombotic occlusion of middle cerebral artery (MCA). T2-weighted, perfusion-weighted (PW), and diffusion-weighted (DW) MR imaging was performed 1 hour and 24 hours after occlusion. On the basis of PW and DW images at 1 hour, 49 rats with cortex and subcortex involvement and with perfusion-diffusion mismatch were randomly assigned into one of four groups: control group, group treated with 7.5 mg microplasmin, group treated with 10 mg/kg microplasmin, or group treated with 10 mg/kg tPA. Agents were intravenously injected 1.5 hours after occlusion. Infarct size and hemorrhagic transformation were assessed with MR imaging and histomorphologic findings. Neurologic deficit was scored. Measurements were statistically analyzed. RESULTS: There were 13 rats in the control group, 13 in the 7.5 mg/kg microplasmin group, nine in the 10 mg/kg microplasmin group, and 14 in the 10 mg/kg tPA group. Despite similar baseline perfusion-diffusion mismatch, histochemically defined total infarct volume was reduced from 25% +/- 5 (standard deviation) in control group to 21% +/- 2, 20% +/- 4, and 20% +/- 5 in 7.5 mg/kg microplasmin, 10 mg/kg microplasmin, and tPA groups, respectively, as similarly shown on T2-weighted, DW, and PW images at 24 hours (P < .05). Cerebral hemorrhage rate at 24 hours was higher in tPA group than in the other three groups. Bederson score of neurologic deficits was significantly reduced in treated groups compared with that in control group. CONCLUSION: Perfusion-diffusion mismatch appeared useful in selecting candidates for thrombolytic therapy. Multiparametric MR imaging allowed noninvasive assessment of effects of microplasmin and tPA in rats; microplasmin had a significantly lower hemorrhagic rate.     

Significance of the perfusion-diffusion mismatch in chronic cerebral ischemia

PURPOSE: To determine whether the perfusion deficit could predict brain infarction in patients with chronic cerebral ischemia who experienced recurring episodes of neurological symptoms and showed a perfusion-diffusion mismatch on magnetic resonance (MR) images. MATERIALS AND METHODS: In 53 consecutive patients (38 males and 15 females, 62+/-13 years old) with ischemia in the middle cerebral artery (MCA) territory, lesion volumetry was performed on parametric maps of the time-to-peak, the cerebral blood volume, and diffusion-weighted (DW) images. The infarct lesions were assessed on follow-up T2-weighted (T2W) MR images after eight days. Cerebrovascular changes were determined by time-of-flight (TOF) MR angiography (MRA). Inferential and correlation statistics were used. RESULTS: Patients with chronic ischemic brain disease (N=39) who presented with a severe perfusion-diffusion mismatch in the presence of a normal cerebral blood volume had no or small brain infarctions as found on follow-up T2W images. MRA revealed widespread abnormalities of the basal cerebral arteries compatible with brain perfusion abnormalities. In contrast, in acute stroke patients (N=14) the deficit of cerebral perfusion predicted the infarct lesion in the T2W images. CONCLUSION: Our results suggest that in chronic cerebral ischemia the normal blood volume was maintained despite the depression of cerebral perfusion and recurring minor insults.     

法舒地尔预处理对大鼠脑缺血再灌注损伤细胞色素C和caspase-3表达的影响

目的研究法舒地尔对大鼠局灶性脑缺血再灌注损伤细胞色素C（CytC）和caspase-3蛋白表达的影响,探讨其脑保护机制。方法线栓法制作大鼠中动脉缺血再灌注损伤模型。成年雄性SD大鼠120只随机分成3组：假手术组（Sham组）、脑缺血再灌注模型组（Mod组）、法舒地尔干预组（Fas组）,再分为再灌注3h、12h、24h和48h,以及TTC染色组5个亚组,每组8只大鼠。缺血再灌注后进行神经功能缺损评分（NDS）,免疫组织化学方法检测脑组织中CytC蛋白、cas-pase-3的表达,TTC染色测量鼠脑梗死体积并计算百分比。结果①Sham组大鼠无神经功能缺损,NDS评分为0,TTC染色亦未见脑组织梗死;Mod组和Fas组大鼠均有明显的神经功能缺损,TTC染色亦可见明显的脑组织梗死;但与Mod组相比,Fas组神经功能缺损少、NDS评分低（P〈0.01）,脑梗死体积减小（P〈0.05）。②与Sham组相比,脑缺血再灌注后,Mod组和Fas组大鼠脑组织CytC和caspase-3的表达显著升高（P〈0.01）,其中CytC表达高峰出现在12h,caspase-3表达高峰出现在24h;Fas组和Mod组间比较显示Fas组CytC和caspase-3的表达又显著低于Mod组（P〈0.01）。结论①法舒地尔能减轻大鼠脑局灶性缺血再灌注引起的神经功能缺损,减小脑梗死体积。②部分抑制脑缺血再灌注引起的CytC和caspase-3表达增加可能是法舒地尔的脑保护机制之一。     

纳络酮对脑梗死大鼠脑损伤的保护作用及对能量代谢的影响

 目的 观察纳络酮对脑缺血再灌注大鼠脑损伤的保护作用及对能量代谢的影响.方法 采用线栓法建立大鼠局灶性脑缺血-再灌注模型,给予纳络酮后测定大鼠脑梗死面积、神经行为评分、脑含水量;制作脑组织匀浆测定脑组织中丙二醛(MDA)含量、超氧化物岐化酶(SOD)活性,并用HPLC测定脑组织ATP含量和能量负荷值.结果 给予纳络酮后大鼠脑梗死面积显著缩小,神经行为障碍显著改善,脑组织水肿得到延缓,丙二醛(MDA)含量显著降低,且脑组织中ATP含量和能荷值显著升高.结论 纳络酮对大鼠局灶性脑缺血再灌注损伤有保护作用,其可能机制在于改善了脑组织的能量代谢.＃     

促红细胞生成素对大鼠脑缺血再灌注后STAT1和STAT3表达的影响及MRI表现

目的探讨促红细胞生成素(EPO)对大鼠局灶性脑缺血再灌注后脑梗死面积变化及信号转导与转录激活子-1(STAT1)、磷酸化STAT1(P-STAT1)、信号转导与转录激活子-3(STAT3)、磷酸化STAT3(P-STAT3)蛋白表达的影响。方法雄性健康SD大鼠40只,随机分为假手术组(A)、脑缺血再灌注组(B)、生理盐水治疗组(C)、EPO治疗组(D),采用线栓法阻断大鼠一侧大脑中动脉血流2 h,再灌注24 h,建成局灶性脑缺血再灌注损伤模型。治疗组于脑缺血刚开始时腹腔注射EPO或等量生理盐水,于24 h时行MRI检查观察脑梗死面积,采用Western blotting检测STAT1、P-STAT1、STAT3、P-STAT3蛋白表达水平的变化。结果与B、C组相比,D组脑梗死面积减小(P<0.05),STAT3磷酸化水平增加(P<0.05),STAT1磷酸化水平有所减少。结论 EPO可能通过影响JAK/STAT信号转导通路减小脑梗死面积。