Meta-analysis of Buyang Huanwu decoction in animal model of cerebral ischemia

Objective:To evaluate the clinical efficacy of Buyang Huanwu decoction in treating animal model of cerebral ischemia.Methods:We searched PubMed,EMbase,Cochrane,CNKI,VIP,WanFang(1983 to 2021)for randomized control trials about Buyang Huanwu decoction treating animal model of cerebral ischemia.Results:According to the inclusion and exclusion criteria and assessment the quality of included trials(RCTs),the extraction of effective data,7 randomized clinical trials and their efficiency were evaluated,statistical analysis was conducted by using RevMan 5.3 software.The outcome measures assessed were neurological score and/or infarction volume.Meta-analysis showed that the neurological behavior scores of Buyang Huanwu decoction on animal model of cerebral ischemia was lower than the control group(SMD=2.06,95%CI(1.75,2.37),P<0.00001);The cerebral infarct volume of Buyang Huanwu decoction on animal model of cerebral ischemia were smaller than the control group(SMD=4.08,95%CI(3.57,4.58),P<0.00001).Conclusion:It was effective by using Buyang Huanwu decoction to reduce neurological behavior scores and the volume of animal model of cerebral ischemia.

Hydrogen sulfide intervention in focal cerebral ischemia/reperfusion injury in rats

The present study aimed to explore the mechanism underlying the protective effects of hydrogen sulfide against neuronal damage caused by cerebral ischemia/reperfusion. We established the middle cerebral artery occlusion model in rats via the suture method. Ten minutes after middle cerebral artery occlusion, the animals were intraperitoneally injected with hydrogen sulfide donor compound sodium hydrosulfide. Immunofluorescence revealed that the immunoreactivity of P2X7 in the cerebral cortex and hippocampal CA1 region in rats with cerebral ischemia/reperfusion injury decreased with hydrogen sulfide treatment. Furthermore, treatment of these rats with hydrogen sulfide significantly lowered mortality, the Longa neurological deficit scores, and infarct volume. These results indicate that hydrogen sulfide may be protective in rats with local cerebral ischemia/reperfusion injury by down-regulating the expression of P2X7 receptors.

Animal models of stroke

Stroke is a devastating disease with high morbidity and mortality.Animal models are indispensable tools that can mimic stroke processes and can be used for investigating mechanisms and developing novel therapeutic regimens.As a heterogeneous disease with complex pathophysiology,mimicking all aspects of human stroke in one animal model is impossible.Each model has unique strengths and weaknesses.Models such as transient or permanent intraluminal thread occlusion middle cerebral artery oc-clusion(MCAo)models and thromboembolic models are the most commonly used in simulating human ischemic stroke.The endovascular filament occlusion model is characterized by easy manipulation and accurately controllable reperfusion and is suitable for studying the pathogenesis of focal ischemic stroke and reperfusion in-jury.Although the reproducibility of the embolic model is poor,it is more conveni-ent for investigating thrombolysis.Rats are the most frequently used animal model for stroke.This review mainly outlines the stroke models of rats and discusses their strengths and shortcomings in detail.

Angiogenesis and neural progenitor proliferation induced by intracarotid administration of mesenchymal stem cells in rats with cerebral ischemia

To investigate the mechanisms of bone marrow mesenchymal stem cells (MSCs) transplantation on neurological function following focal cerebral ischemia in rats.Methods Forty Sprague-Dawley rats, subjected to middle cerebral artery occlusion (MCAo) for 2 hours by intraluminal vascular occlusion, were divided into MSC transplantation group (TG) and cerebral ischemia control groups (CG) at random. MSCs were administrated via carotid artery at 24 hours after MCAo in T groups. At 1, 2, 4 and 12 weeks after MCAo, rats were killed in batches to investigate dynamically the regeneration of microvessels and proliferation of neuronal progenitors in ischemic region by immunohistochemistry and in situ hybridization.Results ①Notable microvessel proliferation in the injured cortex was found 1 week after MCAo and peaked at 2 weeks, then decreased at 4 and 12 weeks. The microvessel density (MVD) in the focal cortex of rats treated with MSC was significantly higher than that of C groups at 1,2,4 and 12 weeks after MCAo (P<0.05). Plenty of VEGFmRNA positive signals were found in cortical and perivascular neurons at 1 and 2 weeks after MCAo, and were more intensive in the T groups than those in C groups at 4 and 12 weeks after MCAo. ②At 1 week after MCAo, numerous nestin -positive cells (NPC) in the injured cortex of parietal lobe, caudate putamen, ependyma ,subependymal zone were observed and the NPC count showed the greatest amount of positive cells at the first week after MCAo, decreased at 2 weeks; and at 12 weeks after MCAo, only scanty NPC scattered in the focal cortex of C groups, whereas, in the T groups, the amount of positive cells remained great.The NPC amount of T groups at each time interval was significantly higher than that of C group(P<0.05) . ③At 1 week after MCAo, large amounts BrdU-labeled cells in the ischemic cortex, caudate putamen, ependyma ,subependymal zone were seen and positive-cell count appeared highest at the first week after MCAo, decreased after 2 weeks; and at 4 and 12 weeks , only scanty BrdU positive cells scattered in the focal cortex of C groups, while, in T groups, a number of positive cells could still be seen in the focal cortex.The BrdU positive cell count of the T group was significantly higher than that of the C group at each time interval(P<0.05).Conclusion These results suggest that MSC transplantation can improve neurological function in cerebral ischemic rats through promoting revascularization and proliferation of neuronal progenitors in the injured region.

Angiopoietin-1 mRNA expression in estradiol-treated ovariectomized rats with focal cerebral ischemia after reperfusion

BACKGROUND： Epidemiologic studies have indicated that the incidence of stroke in premenopausal females is lower than in males at the same age, but it significantly rises in postmenopansal females. Estrogen is used clinically to alleviate injury caused by cerebral ischemia, it has been hypothesized that the neuroprotective role of estrogen relates to angiopoietin （Angpt）, which plays an important role in vascularization, vascular remodeling and maturation. OBJECTIVE： To observe and validate the effect of estradiol on angiopoietin-1 （Angptl） mRNA expression in ovariectomized rats with focal cerebral ischemia after reperfusion, so as to explore the molecular mechanisms of estradiol-mediated protection from cerebral ischemic damage. DESIGN, TIME AND SETTING： Randomized, controlled, molecular biology, prospective animal study. The experiment was performed at the Central Laboratory of Chongqing Medical University from September to December 2005. MATERIALS： Fifty healthy female wild type （WT） rats aged 6 months and fifty female rats aged 6 months with knockout of the estrogen-alpha receptor gene （ERKO）. METHODS： WT rats and ERKO rats were divided into estradiol and control groups （n = 25）, and injected intramuscularly with estradiol benzoate （100μg/kg per day） or corn oil （l mL/kg per day） for 7 days, 30 days after bilateral ovariectomy. Rat models of cerebral ischemia/reperfusion were established with the middle cerebral artery occlusion method. After 30 minutes of middle cerebral artery occlusion, rats from the estradiol and control groups were injected intramuscularly with estradiol benzoate or corn oil at the above dose. MAIN OUTCOME MEASURES： We used radio-immunity analysis and laser-Doppler flowmetry to measure plasma estradiol levels and changes in cerebral blood flow. We used immunohistochemical staining of CD34 epitopes to measure changes in the capillary density in brain following cerebral iscbemia/reperfusion, and quantitative RT-PCR analysis to assess mRNA expression levels of Angptl, Angpt2, Tie2, vascular endothelial growth factor （Vegf）, VegfR1, and Veg, fR2. RESULTS： In WT ovariectomized rats treated with estradiol, the change in cerebral blood flow following cerebral ischemia/reperfusion, capillary density in the basal nuclei and parietal lobe cortex and Angptl mRNA level were significantly higher than in the control group （P 〈 0.01 ）. We did not identify any such changes in ERKO rats treated with estradiol. In addition, the plasma estradiol levels in WT and ERKO ovariectomized rats treated with estradiol were remarkably higher than in their corresponding control groups （P 〈 0.01）. CONCLUSION： Angptl is a critical factor in many processes during the repair of cerebral ischemia/reperfusion injury. For example, it confers estrogen-mediated protection, restoration of cerebral blood flow and increases in brain capillary density. It is emerging as an important molecule for estradiol-mediated neuroprotection.

电凝法与线栓法制备大脑中动脉缺血模型在脑卒中后中枢痛研究中的应用对比

目的采用电凝法与线栓法分别造成小鼠大脑中动脉缺血,建立脑卒中后中枢痛(central post-stroke pain,CPSP)模型,探究更贴近临床的造模方法。方法选择6~8周龄(20~25g)健康雄性C57BL/6小鼠,随机分为空白对照组(Naive组)、电凝组(dMCAO组)和线栓组(tMCAO组),进行不同造模处理。在造模后行Longa神经功能缺陷评分,利用TTC染色评估大脑梗死体积,通过机械性缩足阈值和热缩足潜伏期评估小鼠的疼痛状态,旷场实验评估小鼠的运动功能。结果与Naive组相比,电凝组和线栓组小鼠造模后神经功能缺陷评分均升高(均P<0.01),TTC染色可观察到不同程度的脑缺血(P<0.05,P<0.01);与Naive组相比,电凝组和线栓组在造模后的第7、14、21、28天均表现出机械性痛觉超敏和热痛觉过敏,两组差异无统计学意义;与Naive组相比,电凝组小鼠在造模后第29天的运动功能无显著差异,而线栓组小鼠的运动功能下降(P<0.01)。结论电凝法和线栓法均可诱发脑卒中后中枢痛,但电凝法更贴近CPSP的临床表征,更具复制意义。

阿托伐他汀预处理对高血糖诱导小鼠脑缺血后出血转化的影响

目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红染色观察脑组织出血情况,免疫荧光染色评估血脑屏障通透性,Western blot检测缺血半暗带脑组织免疫球蛋白G(IgG)、闭锁连接蛋白1(ZO-1)、闭合蛋白(occludin)、紧密连接蛋白5(claudin5)、基质金属蛋白酶(MMP)2和MMP-9的蛋白表达。结果与假手术组比较,HT模型组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度、IgG、MMP-2、MMP-9蛋白表达水平显著增高,ZO-1、occludin、claudin5蛋白表达水平明显降低(P<0.01)。与HT模型组比较,阿托伐他汀组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度及IgG、MMP-2、MMP-9蛋白表达水平显著降低[(2.73±1.19)分vs(3.91±0.94)分,16.7%vs 41.6%,58.3%vs 91.6%,(1.00±1.04)分vs(2.58±1.13)分,(504.30±105.52)a.u vs(859.91±153.28)a.u,4.55±1.40 vs 12.06±3.73,1.87±0.41 vs 2.95±0.68,1.47±0.24 vs 2.12±0.23,P<0.05,P<0.01],ZO-1、occludin、claduin5蛋白表达显著升高(1.55±0.20 vs 0.53±0.10,0.92±0.11 vs 0.35±0.07、0.58±0.04 vs 0.30±0.05,P<0.01)。结论阿托伐他汀可通过抑制MMP-2、MMP-9激活,上调ZO-1、occludin、claudin5表达,降低血脑屏障通透性,从而抑制高血糖诱导的脑缺血后HT。

蛛网膜下腔出血的脑损伤机制及相关生物标志物研究进展

蛛网膜下腔出血(SAH)是一种严重的急性出血性脑卒中,具有极高的致死率和致残率。出血后发生脑损伤的机制主要包括早期脑损伤和迟发性脑缺血,最终会导致预后不良。目前,治疗并减轻脑损伤的措施有限。在此,笔者回顾了SAH动物模型及SAH后脑损伤的病理机制,并总结了相关的生物标志物在脑损伤及预后不良中的作用,以期为SAH的药物研发及临床治疗方案制订提供思路。

改良的四血管间断阻塞法制作大鼠全脑缺血再灌注损伤模型

目的改良Pulsinelli与Brierley建立的经典四血管阻塞(4VO)模型。方法80只雄性SD大鼠。其中32只随机分为:假手术组、I4VO-Con10组、I4VO-Int10组和I4VO-Int15组。假手术组暴露双侧椎动脉与颈总动脉但不夹闭;I4VO-Con10为持续缺血组,夹闭双侧椎动脉与颈总动脉10 min,再灌注24 h;I4VO-Int10组和I4VO-Int15组为间断缺血组,I4VO-Int10组进行5 min缺血、5 min再灌注及5 min缺血,然后再灌注24 h;I4VO-Int15组缺血5 min、再进行2次5 min/5 min的再灌注/缺血循环,随即再灌注24 h。激光多普勒监测局部脑血流量,观察大鼠生存情况,HE染色观察海马组织病理改变,以此确定最优改良方法;48只大鼠按照最优改良方法(I4VO-Int15)建立I4VO模型,随机分为假手术组和5个I4VO模型组。5个I4VO模型组根据再灌注时间点(1、3、7、14、28 d)分为I4VO-D1、I4VO-D3、I4VO-D7、I4VO-D14和I4VO-D28组。记录各组大鼠体质量与生存状况,HE染色观察海马、视网膜与视束形态学改变;Y迷宫实验、明暗箱实验评估I4VO-D28组大鼠认知功能与视功能。结果I4VOInt15是最优改良方法;I4VO-D1组、I4VO-D3组、I4VO-D7组、I4VO-D14组和I4VO-D28组体质量较对应时间点假手术组的体质量明显降低,存活率无显著性差异,海马神经元损伤、丢失进行性加重;I4VO-D28组大鼠出现认知障碍;I4VO-D28组大鼠视网膜、视束未见明显缺血性损伤。结论改良的I4VO模型能够成功复制大鼠全脑缺血再灌注损伤的主要病理过程;改良的I4VO模型未引起视功能损伤。

高糖诱导小鼠脑缺血后出血转化的研究

目的 探讨稳定的高糖诱导小鼠脑缺血后出血转化模型的实验条件。方法 采用线栓法制备小鼠大脑中动脉闭塞模型,将小鼠按照葡萄糖浓度(10%,20%,30%,40%,50%)与缺血时间(30 min, 1、2、3 h)进行组合,每个浓度4个时间点,共分为20组合,每组6只。术前15 min腹腔注射不同浓度葡萄糖,分别在脑缺血术后30 min, 1、2、3 h拔出线栓恢复再灌注,诱导小鼠脑缺血后出血转化模型。以术后24 h内死亡率以及术后7 d内脑出血大体观察,脑皮质和白质出血量,出血发生率及死亡率为指标。结果 大体观察显示,随着缺血时间延长或葡萄糖浓度升高,脑组织出血发生率呈逐渐上升趋势。苏木精-伊红染色镜下观察显示,大部分模型组合小鼠随着缺血时间延长或葡萄糖浓度升高,大脑白质及皮质内出血量呈逐渐上升趋势。术后7 d内,葡萄糖浓度升高或缺血时间延长均增加模型小鼠出血发生率,差异有统计学意义(F=15.282,F=6.632,P<0.01)。术后24 h和术后7 d内,葡萄糖浓度升高或缺血时间延长均显著增加模型小鼠死亡率,差异有统计学意义(P<0.05,P<0.01)。结论 当葡萄糖浓度为30%,缺血时间为30 min时,高糖诱导可制备死亡率低,出血转化发生率高的脑梗死后出血转化模型。

线栓法与化学损毁法造模引起模型大鼠吞咽功能损害的对比

背景:建立动物模型是研究卒中后吞咽障碍的重要研究方法之一,线栓法是缺血性脑卒中最常用的经典模型,新近研究表明,化学损毁吞咽中枢疑核也能造成大鼠表现吞咽功能障碍,但其造模成功率、临床相似性、可调控性仍不确定。目的:观察线栓法与化学损毁法两种不同造模方法对大鼠模型的吞咽功能改变,探究能较完整表现与人类相似的吞咽障碍临床及病理特征。方法:将40只SD大鼠随机分为3组,正常组10只,线栓组15只,化学损毁组15只,线栓组以线栓法短暂脑缺血90 min后再灌注制备左侧卒中脑缺血模型,化学损毁组以鹅膏蕈氨酸化学损毁疑核造成大鼠吞咽障碍模型。记录各组大鼠每周存活数、体质量及24 h进食、进水量,在造模后第2,7,14,30天时采用生物信号采集器及张力换能器检测大鼠吞咽启动反应时间及吞咽次数,并采用苏木精-伊红染色观察延髓吞咽中枢疑核处病理学形态变化,ELISA法观察各组大鼠血清的白细胞介素6、白细胞介素1β、肿瘤坏死因子α的表达变化。结果与结论:①和化学损毁组相比,线栓组大鼠死亡率在第2,7天显著降低(P<0.05),其余时间段无明显差异(P>0.05),且线栓组最终死亡率明显低于化学损毁组(40%,73%,P<0.05);②与正常组相比,造模后第7天化学损毁组大鼠体质量及24 h进食、进水量均减少、吞咽启动反应时间延长、吞咽次数减少,差异均有显著性意义(P<0.05),线栓组无明显差异(P>0.05);与正常组相比,第14天后2个造模组大鼠体质量及24 h进食、进水量均减少,吞咽启动反应时间均延长,吞咽次数均减少,差异均有显著性意义(P<0.05);线栓组和化学损毁组相比,大鼠体质量及24 h进食、进水量、吞咽启动反应时间、吞咽次数在第7天差异有显著性意义(P<0.05),其余时间段无明显差异(P>0.05);③2个造模组大鼠的延髓处均较出现明显病理性改变,延髓处炎症细胞均明显增多;线栓组和化学损毁组相比,病理性改变不明显;④提示无论是线栓法和化学损毁疑核法都可引起大鼠吞咽功能改变;线栓组的死亡率在造模后的所有时间段内均低于化学损毁组,从模型最终的成功率而言,线栓法短暂脑缺血90 min后再灌注大鼠模型更具复制意义。

Altered expression of bcl-2 mRNA and Bax in hippocampus with focal cerebral ischemia model in rats

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光化学诱导老年大鼠局灶性脑梗塞模型的研究

目的 探讨年龄对脑缺血的影响 ,建立一个稳定的、与人类卒中年龄相关的老年大鼠局灶性脑缺血模型。方法 采用Watson法制作光化学脑缺血模型 ,对比观察老年鼠及青年鼠缺血诱导后血脑屏障、梗塞灶大小及光镜、电镜下缺血区的病理变化。结果 (1 )缺血诱导的大鼠存活率 1 0 0 % ,梗塞灶恒定出现。 (2 )与青年鼠相比 ,缺血老年鼠的精神差、血脑屏障破坏重、梗塞灶大 ,神经细胞受损、炎性细胞浸润严重而胶质细胞及微血管增生等组织修复反应轻。结论 同等缺血打击下 ,老年鼠的缺血性损害重、修复能力低。光化学诱导老年大鼠局灶性脑梗塞模型稳定性好、死亡率低 。

大鼠局灶性脑缺血模型制作方法的改进

目的 探索导致栓线法局灶性脑缺血模型制作失败的原因,提出相应的技术解决方法。方法 按照文献方法,采用体重为250-350 g的SD大鼠进行栓线法局灶性脑缺血模型制作。结果在模型制作过程中,遇到的最大困难是栓线插线时的大出血,以及有时栓线无法正确插入颈内动脉。不用血管夹夹闭颈内、外动脉,直接在颈内动脉靠近分叉处套上一根丝线,用血管钳牵拉,就可以很容易地控制出血;遇到栓线插入困难时,向深层次解剖,显露翼腭动脉和颈内动脉分叉,就可以直视下将栓线插入颈内动脉。结论 采用预先在颈内动脉套线,可以方便有效地控制出血。插线困难时,向深部解剖显露翼腭动脉后可以在直视下将栓线送入颈内动脉,无需结扎翼腭动脉。整个手术操作可以由一个人完成。

半胱氨酸蛋白酶抑制剂对大鼠脑缺血模型DNA损伤的实验研究

目的研究caspase-3抑制剂Ac-DEVD-CMK及calpain抑制剂ALLN干预治疗对大鼠局灶性脑缺血/再灌注模型的神经保护作用。方法经左侧侧脑室注射DEVD或/和ALLN及溶剂二甲基亚砜(DMSO)后,制作大鼠左侧MCA缺血再灌注模型;缺血2h再灌注24h进行TTC染色观察梗死灶的形成情况;并分别于缺血2h再灌注24h或48h检测鼠脑中单、双链DNA断裂情况。结果溶剂DMSO预处理组的各项指标与MCAO模型组无明显差异;DEVD或ALLN治疗后缺血侧脑中Klenow及TUNEL阳性细胞数均明显减少,二者合用作用最强。结论Caspase-3与calpain均在缺血性脑损伤中起重要作用,对此进行治疗干预具有潜在的临床应用价值。

多因素复合制作气虚血瘀证脑缺血动物模型的实验研究

目的 通过复制气虚血瘀证型大鼠脑缺血动物模型 ,探索病证结合动物模型制作方法。方法 选用老年Wistar大鼠 ,采用饥饿、疲劳、寒湿、惊恐、高脂饮食等多因素复合方法复制气虚血瘀证动物模型 ,采用双侧颈总动脉结扎复制脑缺血动物模型。结果 通过对一般体征和微观指标的观测 ,发现模型大鼠基本符合中医气虚血瘀证候特点和现代医学脑缺血病理变化规律。结论 多因素复合作用可成功复制病证结合动物模型 。

改良线栓法制备大鼠局灶性脑缺血/再灌注模型

目的建立一种简便可靠、创伤较小的大鼠局灶性脑缺血/再灌注模型。方法对Zea Longa线栓法进行适当改进,制作SD大鼠右侧大脑中动脉闭塞(MCAO)2 h后再灌注(R)模型(MCAO/R组,n=25)。于建模前后不同时间点,评估SD大鼠的神经功能;建模后14 d处死所有大鼠,取脑组织进行病理组织学检查。设立假手术组(n=5)作为对照,进行对比分析以观察模型的可靠性。结果MCAO/R组25只大鼠中,2例(8%)于拔栓线时突发死亡,迅速开颅取脑发现颅底脑池内有大量血块;2例于术后第2天死亡,1例于术后第7天死亡,总死亡率为20%。成功建立MCAO/R模型20例,并在为期14 d的观察过程中神经功能逐渐改善;术中栓线插入长度与大鼠体质量呈线性相关(P=3.86×10-9);组织病理学观察显示,MCAO/R组大鼠的右侧额顶叶和尾壳核区域脑组织缺血性损伤改变,神经元皱缩,呈不规则形态;胞浆嗜酸性,胞核深染或消失,细胞间质疏松。结论本实验采用改良线栓法制备的大鼠MCAO/R模型,简便易行、创伤小且稳定性好,是用于研究局灶性脑缺血/再灌注损伤较为理想的动物模型。

颈动脉负压分流制作大鼠全脑缺血/再灌注模型

目的 根据解剖学和血流动力学原理建立新型大鼠全脑缺血 再灌注模型。方法 夹闭大鼠双侧颈总动脉 ,同时经右颈外动脉持续抽吸颈总动脉内血液 ,造成大鼠全脑缺血 ,抽出的血液从左股静脉回输 ;停止抽吸血液 ,去除微动脉夹 ,开始再灌注。应用脑电图、光镜和电镜等评定脑缺血的效果。结果 实验组大鼠脑电图、光镜和电镜检查均显示明显的缺血改变。结论 本模型具有全脑缺血效果可靠、再灌注充分、制备简便、成功率高并可经颈动脉注入药物等优点 ,适用于全脑缺血

大鼠局灶脑缺血再灌注模型的研究

对尼龙线栓塞大鼠大脑中动脉的局部脑缺血再灌注模型进行研究。观察了大鼠脑缺血不同时间再灌注的成功率、脑水肿、神经病学评分及血流量（ｒＣＢＦ）的动态变化。结果如下：（１）改进实验方法后，使大鼠脑缺血不同时间再灌注的成功率明显提高；（２）脑缺血后早期再灌注，可显著降低脑水肿，改善神经损伤症状；（３）大鼠脑缺血期ｒＣＢＦ降至正常值的１５．７％～１９．１％。再灌后，ｒＣＢＦ恢复至正常值的５９．４％～８４．９％。

局灶性脑缺血再灌注动物模型的制备及评价

目的 :研究局灶性脑缺血再灌注动物模型在缺血 90 ,12 0 ,180min恢复再灌后对脑梗死体积和行为学方面的影响。方法 :采用线栓法建立SD大鼠局灶性脑缺血再灌注模型 ,并将其分为假手术对照组、缺血 90 ,12 0和180min再灌组共 4组。用盐酸 2 ,3,5 三苯基四氮唑 (TTC)染色法测定脑梗死体积和神经功能评分法评价其行为学。结果 :TTC染色显示该模型的缺血区主要位于视交叉后 2～ 4mm脑皮质。缺血 90min再灌组、缺血 12 0min再灌组和缺血 180min再灌组脑梗死体积差异无统计学意义 ,缺血 12 0 ,180min再灌组 2组脑梗死体积较 90min再灌注组有增加趋势 ,3组行为学改变以再灌注后 3～ 6h最明显。结论 :选择脑缺血 12