自体血栓和凝血酶致大鼠局灶性脑梗死模型的建立与应用

目的 建立自体血栓和凝血酶致大鼠局灶性脑梗死模型。方法 采用经颈外动脉向颈内动脉注入自体血栓和凝血酶栓塞大鼠大脑中动脉的方法,建立局灶性脑梗死模型并观察重组葡激酶（rSak）对该模型的改善作用。结果 注入10 μL自体血栓和50 U凝血酶时大鼠脑血流量较基础值降低,出现严重脑梗死神经症状、较大脑梗死范围和明显病理学改变,为理想模型。rSak 150 kU/kg能提高脑血流量,减少脑神经缺陷评分,缩小脑梗死范围,减轻病理学改变。结论 建立了经颈内动脉注入自体血栓和凝血酶致大鼠局灶性脑梗死模型,并用rSak验证了该模型的稳定性及可靠性。     

大鼠自体血血栓脑缺血模型建立光镜和电镜观察

目的：大鼠脑缺血模型的建立,探讨脑梗死组织生理、病理变化,研究治疗对策。方法：采用HE染色和电子显微镜观察大鼠自体血脑梗死模型。结果：光镜下示大脑皮层,基底节区、海马、软组织均有神经细胞变性、坏死,蛛网膜下腔有微血栓形成。电镜示梗死区细胞肿胀,胞质稀少。结论：鼠自体血血栓制作更接近人体血栓,缺血严重时可引起脑细胞不可逆性损伤,应加强脑缺血早期防治。     

瑞替普酶溶栓治疗脑梗死的疗效研究

目的观察瑞替普酶(rPA)对大鼠脑梗死模型的溶栓作用,为临床应用rPA溶栓治疗脑梗死提供实验依据。方法通过大鼠颈内动脉注入自体血栓栓塞大脑中动脉起始部,1.5h后36只大鼠采用rPA溶栓治疗,24h后观察溶栓效果。结果治疗组与对照组相比Longa评分降低(P<0.01),梗死体积减少(P<0.01),细胞形态结构完整。结论rPA早期溶栓治疗大鼠急性脑梗死可显著减小梗死体积、改善神经功能缺失症状、降低死亡率,且应用方便;rPA在临床脑梗死的溶栓应用可能同样有效。     

小鼠局灶性脑缺血再灌注模型的建立与评价

目的 建立小鼠局灶性脑缺血再灌注（I/R）模型并予以评价.方法 将昆明小鼠60只随机分为假手术组30只,I/R模型组30只.改良线栓法制备小鼠大脑中动脉阻塞/再灌注（MCAO/R）模型.通过神经行为学评分、氯化三苯基四氮唑（TTC）染色法测定脑梗死比（％）、干湿重法测定脑含水量（％）及HE染色观察脑组织病理改变评价模型可靠性.结果 模型存活率为83.33％,造模总成功率为76.67％.假手术组的小鼠神经行为学评分为0分,脑梗死比为0,脑含水量（77.29±0.45）％.I/R模型组的小鼠神经行为学评分为（2.42±0.63）分,脑梗死比为（23.03±3.42）％,脑含水量（83.18±1.65）％,均较假手术组明显增高（P＜0.01）;病理检查出现典型脑梗死病理改变.结论 改良线栓法成功建立简便、可靠的小鼠局灶性I/R模型.     

臭氧自体血回输治疗急性脑梗死的临床分析

目的 (1)观察臭氧自体血回输治疗急性脑梗死的临床疗效。(2)观察臭氧自体血回输治疗对急性脑梗死患者血脂的影响。方法将80例急性脑梗死患者随机分为治疗组和对照组各40例,两组均进行基础用药治疗,治疗组在此基础上加用臭氧自体血回输治疗,每周2次,共5次,分别在入院时和14 d后进行神经功能缺损评分及观察血脂的变化。结果治疗组脑梗死治疗总有效率高于对照组,治疗组血脂下降水平高于对照组。结论与对照组相比臭氧自体血回输疗法能减轻急性脑梗死患者神经功能缺损程度,降低致残率,疗效显著。     

米非司酮对子宫内膜异位症大鼠的治疗作用及对COX-2及VEGF表达的影响

目的 探讨米非司酮对子宫内膜异位症(endometriosis,EMS)大鼠的治疗作用及对环氧合酶-2(COX-2)、血管内皮生长因子(vascular endothelial grewth factor,VEGF)表达的影响.方法 采用自体移植法建立EMS大鼠模型,随机分为模型组、低、中、高剂量组,各10只,另设假手...     

芪冬颐心口服液对脑梗死大鼠神经保护作用的实验研究

目的 研究芪冬颐心口服液对脑梗死大鼠的神经保护作用。方法 50只雄性SD大鼠随机分为假手术、模型组、芪冬颐心口服液高、中、低剂量组,于脑梗死模型建立后2h给药干预,连续给药14d,观察芪冬颐心口服液对脑梗死大鼠神经功能、脑组织SOD(超氧化物歧化酶)、MDA(丙二醛)及神经凋亡相关蛋白Bcl-2表达的影响。结果 与模型组比较,芪冬颐心口服液高、中、低剂量组能显著改善神经功能情况、提高脑组织中SOD含量,降低MDA含量,并抑制Bcl-2蛋白的表达(P<0.05,P<0.01)。结论 芪冬颐心口服液对脑梗死大鼠具有一定的神经保护作用。     

胶原酶与自体血建立脑出血模型的比较研究

目的比较胶原酶脑出血模型与自体血脑出血模型的稳定性。方法分别采用胶原酶和自体血注入大鼠尾状核建立脑出血模型,比较两组模型死亡率、神经功能缺陷评分、脑组织水含量、血肿大小、神经元细胞凋亡的差异。结果假手术组术后神经功能缺陷评分、脑水含量、血肿体积、神经元细胞凋亡数量未见明显变化;胶原酶组成功率高于自体血组(P<0.05);两组死亡率基本一致。胶原酶模型组24 h、3 d、7 d时间点神经功能缺陷、脑水含量、血肿体积、神经元细胞凋亡数量均明显高于自体血模型组(P<0.05)。结论胶原酶脑出血模型较自体血脑出血模型稳定。     

疏血通注射液对局灶性脑缺血大鼠的治疗作用

目的:观察疏血通注射液治疗局灶性脑缺血大鼠脑梗死的效果。方法:采用自体血栓注入并闭塞大脑中动脉的方法,制备局灶脑缺血模型。假手术组、大脑中动脉闭塞(MCAO)模型组(模型组)大鼠尾静脉注射生理盐水、疏血通治疗组大鼠尾静脉注射疏血通注射液,均0.25mL·kg-1,qd,连续5d。观察3组大鼠的脑梗死范围、脑含水量、神经功能评分、血管闭塞和再通情况、病理组织学改变等指标的变化。结果:模型组大鼠脑含水量(84±s3)%,比假手术组(74±3)%明显增多;疏血通注射液可明显改善神经功能缺失评分,缩小脑梗死范围,降低脑组织含水量,此外疏血通注射液还可促进血栓溶解,使血管再通并减轻脑组织病理变化。结论:疏血通注射液对局灶性脑缺血大鼠急性脑梗死有明显的治疗作用。     

4类材料包裹治疗犬梭形动脉瘤的高频超声观察与病理学评价

目的 探讨生物膜等4类材料包裹治疗犬梭形动脉瘤(FFA)模型的远期疗效.方法 10只犬的20枚梭形动脉瘤分别用生物膜、自体颈外静脉(EJV)、膨体聚四氟乙烯膜片(e-PTFE)、涤纶片等建立完全匹配包裹模型各5枚,观察建模后血流动力学变化与病理学改变.结果 随建模时间延长,EJV降解、模型膨胀性增大,瘤壁机化、钙化、炎...     

CEREBROVASCULAR CONTRACTILITY AFTER CLOT REMOVAL IN MONKEY SUBARACHNOID HAEMORRHAGE

1. The effects of mechanical clot removal during early surgery on pharmacological cerebrovascular reactivity after subarachnoid haemorrhage (SAH) were investigated in the monkey. 2. Contractions to potassium chloride, 5-hydroxytryptamine and noradrenaline in rings of proximal parts of middle cerebral arteries (MCP), surrounded with clot, and basilar arteries (BAP), far from the clot, were examined 7 days after SAH, in which an autologous blood clot was bilaterally placed around major cerebral arteries. 3. Compared with the sham-operated group, contractions in the clot removal groups at 48 and 72 h after SAH were reduced in MCP and enhanced in BAP. 4. These results suggest that divergent vascular contractility may occur according to the distance between artery and clot if the clot is removed later than 48 h after SAH.     

南苜蓿总皂苷对麻醉犬脑血流动力学的影响

目的:观察南苜蓿总皂苷对麻醉犬脑血流量、脑血管阻力的影响。方法:将36只麻醉犬随机分为6组,分别为南苜蓿总皂苷高、中、低剂量组、尼莫地平组、脑心通组、对照组,麻醉后股动脉插管,经压力换能器连接多导生理记录仪,颈总动脉连接电磁血流量计,按相应分组经十二指肠给药,测定给药前后的颈总动脉血流量、收缩压、舒张压、平均动脉压、心率、呼吸次数等变化率,计算脑血流量和脑血管阻力。结果:南苜蓿总皂苷高剂量(0.42 g·kg^-1)能显著增加麻醉犬给药后40,50,70 min的脑血流量变化率并降低给药后40,50,70 min脑血管阻力变化率,同时降低给药后40,70 min的收缩压和舒张压变化率(P<0.05或P<0.01),对心率和呼吸次数无影响。结论:南苜蓿总皂苷通过增加脑血流量,降低脑血管阻力,降低血压,从而改善脑血流动力学指标,防治缺血性脑血管病。     

Effect of lisuride on experimental cerebral infarction in rats]

Lisuride is an ergot derivative with central dopaminergic (D2 agonistic) and serotonergic (5-HT1A agonistic) activity. The effect of lisuride on experimental cerebral infarction in rats was investigated. Cerebral infarction was induced by intracarotid infusion of a 50-microliters mixture in which deformed and rigid red blood cells treated with hypertonic solution were contained. Lisuride or 0.9% NaCl was administered subcutaneously 30 min before induction of cerebral infarction. Lisuride (0.01 mg/kg) not only prolonged the survival time of the animals but also suppressed cerebral edema, increase in the electrolytes content and histological damage in the brain. These results suggest that lisuride has a protective effect against cerebral infarction.     

Inhibitory effect of activated protein C on cerebral vasospasm after subarachnoid hemorrhage in the rabbit

This study investigated whether activated protein C (APC) improves the cerebral vasospasm in an experimental subarachnoid hemorrhage that was produced by the intracisternal injection of autologous blood. Male rabbits were divided into the following four groups: APC 0.1-and 0.5-mg groups, in which 0.1 and 0.5 mg APC were injected into the cisterna magna, respectively; a placebo group, in which saline was injected instead of APC; and a sham operation group that did not get injections of autologous blood, APC, and saline. On day 2, amount of clot in the basal cistern was significantly (p < 0.01) decreased in the APC 0.5-mg group. Percent diameter of the basilar artery on day 2 to that before injecting the blood was angiographically determined as 97.1 +/- 3.8% in the APC 0.5-mg group, which was significantly (p < 0.001) greater than the corresponding value in the placebo group (74.8 +/- 3.4%). The impaired endothelium-dependent relaxation following subarachnoid hemorrhage was normalized in the APC 0.5-mg group (p < 0.0001). These results suggest that APC would improve cerebral vasospasm following subarachnoid hemorrhage, possibly by decreasing the amount of subarachnoid clot and normalizing the impaired nitric oxide production/release.     

Effects of intra-arterial urokinase on a non-human primate thromboembolic stroke model

One of the most important prognostic factors in the thrombolytic treatment of acute ischemic stroke is to re-canalize. The purpose of this study was to evaluate the effectiveness and safety of urokinase in a primate thromboembolic stroke model. Thromboembolic stroke was accomplished via occlusion of the middle cerebral artery (MCA) obtained by injecting an autologous blood clot into the left internal carotid artery in 21 male cynomolgus monkeys. Animals were randomly assigned to the following treatment groups: Group 1: vehicle (saline), Group 2: urokinase (40,000 IU), Group 3: urokinase (120,000 IU,) over 2 or 6 h via intra-internal carotid catheter starting 1 h after embolization, respectively. In the urokinase-treated groups, neurologic deficits were improved in consciousness and skeletal muscle coordination, but not sensory and motor systems. The infarction size in Group 2 (11.9 +/- 3.9% of the hemisphere) and 3 (7.6 +/- 2.5%) were significantly smaller than that (24.7 +/- 3.5%) in Group 1. However, 2 of 5 animals in Group 3 died. In conclusion, urokinase improved neurologic deficits and reduced cerebral infarction on thromboembolic stroke in the cynomolgus monkey.     

脑梗死患者经颅多普勒超声的结果分析

目的分析脑梗死患者的经颅多普勒超声(TCD)结果。方法选取我院2007年6月至2011年5月经TCD检查的脑梗死患者500例,分别经枕窗、颞窗、下颌窗常规检测颈内动脉终末段(ICA)、大脑中动脉(MCA)、大脑前动脉(ACA)、大脑后动脉(PCA)、颈内动脉颅外段(ICAex)、椎动脉(VA)、基底动脉(BA)。结果 500例患者中TCD正常68例(13.6%),异常432例(86.4%),主要为颅内大动脉血流速度增快、减慢、频窗消失、涡流伴杂音等。结论脑梗死患者TCD检查发现部分患者脑血流有显著变化,对脑梗死的治疗及预防提供了一定的参考依据。     

进展性脑梗死46例危险因素的临床探讨

目的 探讨进展性脑梗死的危险因素。方法 选择2011年10月-2013年10月焦作市第四人民医院收治的急性脑梗死患者120例,分为进展性脑梗死组46例与非进展性脑梗死组74例,单因素筛选与Logistic回归分析两组临床一般资料、生化指标监测及影像学检查结果 。结果 分水岭脑梗死（额顶、顶枕、额颞等交界区及侧脑室旁）、颈动脉狭窄≥50％、收缩压、体温升高、血浆纤维蛋白原、D-二聚体是急性脑梗死呈进行性加重的独立危险因素。结论 进展性脑梗死的发生是多种因素、多种机制共同作用的结果 ;临床中发现上述独立危险因素应予积极处理,以减少进展性脑梗死的发生,改善急性脑梗死的治疗效果。     

阿托伐他汀对合并高脂血症脑梗死患者血液流变学的影响

目的观察阿托伐他汀对合并高脂血症脑梗死患者血液流变学的影响。方法 138例合并高脂血症脑梗死患者随机分为常规治疗组(n=69)和阿托伐他汀治疗组(n=69),阿托伐他汀治疗组除进行常规治疗外,加用阿托伐他汀10 mg/d,分别于入院时及临床治疗14 d检测患者的血脂及血液流变学指标,对两组治疗前后血脂及血液流变学指标的结果进行比较。结果阿托伐他汀治疗组治疗后总胆固醇、三酰甘油、低密度脂蛋白降低,高密度脂蛋白增高,全血黏度、血浆黏度、红细胞聚集指数、红细胞刚性指数、红细胞变形指数降低,与对照组对比差别有统计学意义(P<0.05)。结论合并高脂血症脑梗死患者应用阿托伐他汀能起到降低血脂及改善血液流变学作用。     

出血性脑梗死相关危险因素及预后分析

目的研究出血性脑梗死(hemorrhage infarction,HI)的相关危险因素和预后。方法我院948例急性脑梗死住院患者,分析其梗死类型、梗死面积、血糖及溶栓治疗与HI发生的关系,比较出血发生时间、出血类型与短期预后之间的关系。结果脑梗死后出血性转化与梗死机制、梗死面积、高血糖及溶栓治疗有关;其出血性转化发生时间愈早则预后愈差,血肿型预后较非血肿型差。结论脑栓塞、大面积脑梗死、高血糖、溶栓治疗是HI的主要危险因素。     

Beneficial effect of OKY-046, a selective thromboxane A2 synthetase inhibitor, on experimental cerebral vasospasm

Effects of OKY-046, a selective inhibitor of thromboxane (TX)A2 synthetase and a platelet aggregation inhibitor, on in vitro and in vivo models of cerebral vasospasm were studied. The contraction of the isolated rabbit basilar artery by an exposure to 1.0 ml of whole rabbit blood plus 0.05 or 0.1 units/ml of thrombin was diminished by the treatment with 10(-4) M of OKY-046 and/or 10(-6) M of cinanserin. When the whole blood of rabbits treated intravenously with 1 mg/kg/min of OKY-046 was used, the contraction of the basilar artery was decreased to about half of the control contraction. Angiographically recognized cerebral vasospasm in vivo, by a transorbital injection of 5.0 to 7.0 ml of autologous arterial blood into the cisterna magna of dogs, was suppressed by 0.05 and 0.5 microgram of OKY-046. Moreover, the decrease in the regional cerebral blood flow in autologous blood infused-dogs was inhibited by 0.5 microgram of OKY-046. The increase in TXB2 in the cerebrospinal fluid of dogs was significantly inhibited, and the level of 6-keto-PGF1 alpha was slightly increased by the treatment of OKY-046. The ratio of 6-keto-PGF1 alpha/TXB2 was increased from 1.5 to 5.2 in OKY-046-treated dogs. No effect on the basal tone and response to vasoactive agonists such as norepinephrine, KCl and PGE1 was observed in the isolated spiral thoracic aorta of guinea pigs or rabbits. Taken together with our previous findings, we conclude that the inhibition of cerebral vasospasm in the in vitro and in vivo models by the treatment of OKY-046 might be due to an inhibition of platelet aggregation, an inhibition of TXA2 generation and an increase in the ratio of PGl2/TXA2.