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1.
线栓法建立小鼠脑缺血再灌注模型影响因素探讨   总被引:3,自引:1,他引:2  
目的探讨小鼠脑缺血再灌注线栓模型建立的影响因素.方法小鼠90只,根据不同种系、体重等分为三组,经颈总动脉插入线段,将其头端送至左侧大脑中动脉起始部,2 h后拔出线栓,实现再灌注,术后22 h的脑组织切片经2,3,5-氯化三苯基四氮唑(TTC)染色计算梗死灶的大小.结果种系、体重的差异均影响到模型的建立. 结论建立小鼠缺血再灌注模型时必须严格控制以上因素,以适应实验要求.  相似文献   

2.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

3.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

4.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

5.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

6.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

7.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

8.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

9.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

10.
目的 研究大鼠局灶性脑缺血再灌注区域信号转导子与转录激活子-3(STAT3)激活变化,探讨其与梗死面积变化的关系. 方法 99只雄性SD大鼠分为假手术组和缺血2 h、6 h再灌注不同时间组,线栓法建立大脑中动脉闭塞(MCAO)模型.各组动物于不同时间点处死取脑,取相应部位脑组织行TTC染色.采用免疫组化及免疫印迹法检测STAT3蛋白表达和磷酸化水平,分析其与梗死面积变化的相关性. 结果缺血后TTC染色可见部分右侧大脑半球失染呈白色.缺血6h组再灌注0 h较缺血2 h再灌注0 h TTC失染面积大.差异有统计学意义(P<0.05).缺血2 h再灌注24 h后失染面积较灌注0 h明显变小,差异有统计学意义(P<0.05).免疫组化定位:STAT3在胞浆中表达,磷酸化STAT3(P-STAT3)在胞核中表达.Western blot半定量分析结果:缺血再灌注不引起STAT3蛋白表达的变化,但P-STAT3表达增加,随着再灌注时间延长,24 h达到峰值.STATS激活的水平与TTC失染面积变化呈负性相关(缺血2 h组:r=-0.680,P<0.05;缺血6 h组:r=-0.672,P<0.05). 结论 脑缺血再灌注不同时间STAT3表达水平无明显变化,但可诱导缺血区域磷酸化水平增加,其激活水平与梗死面积相关.  相似文献   

11.
大鼠大脑中动脉线栓法的改良与评价   总被引:5,自引:0,他引:5  
目的大鼠大脑中动脉线栓法是一种重要的实验方法,本文介绍对它的改良,并通过神经行为学评分、乳酸脱氢酶活性、红四氮唑染色法与组织病理改变进行评价。方法用头端处理过的尼龙钓鱼线从颈总动脉插入颈内动脉,可逆性地阻断一侧大脑中动脉。结果大鼠大脑中动脉栓塞2h再灌注22h后,大鼠出现明显神经症状;红四氮唑染色清楚显示了梗死病灶;光镜与电镜发现了脑缺血的病理变化。结论该改良方法简单易行,结果可靠,可以用于脑缺血再灌注的研究。  相似文献   

12.
A variety of intraluminal sutures have been used in the middle cerebral artery occlusion model (MCAO) of focal ischemia. In the present study we tested commercially available silicon-coated nylon suture in the MCAO model and compared the results to traditional monofilament nylon suture occlusion. Twelve Sprague-Dawley male rats were randomly divided two groups, MCAO with 4-0 nylon suture (Group N, n=6) and MCAO with silicone-coated 4-0 nylon suture (Group S, n=6). Rats were sacrificed 24 h after reperfusion. Assessment included mortality rates, neurological evaluation, and infarct volume. One rat died in each group from subarachanoid hemorrhage. Neurological evaluation demonstrated that Group S tended to have worse neurological outcomes than Group N, although this difference was not statistically significant. On TTC stain Group S had significantly larger infarct volumes than Group N. We conclude that the commercially available silicone-coated occlusion suture provides better occlusion of the middle cerebral artery than the traditional uncoated nylon suture. Classification: Disease-related neuroscience (Section 6).  相似文献   

13.
Using dogs, we developed an intravascular model for reversible middle cerebral artery occlusion that does not involve intracranial surgery or enucleation. Using silicone plastic plugs with a suture embedded within them, we embolized the middle cerebral artery in 19 dogs via the cervical carotid artery. The free end of the suture remained accessible in the neck, and after variable dwell times traction was placed on the suture and the plug was withdrawn. Placement of the plug in the middle cerebral artery produced ischemia in the basal ganglia. The degree and distribution of cortical ischemia were variable as evidence by the pathologically documented scattered nature of infarcts that resulted when the plug was left permanently in the middle cerebral artery and when it was removed after 1 or 2 hours. Angiography demonstrated occlusion of the middle cerebral artery with the plug in place as well as reperfusion when the plug was withdrawn. This modification of a previously described model of middle cerebral artery occlusion provides an opportunity to study structural, physiologic, and biochemical events occurring in acutely hypoperfused cerebral tissue as well as critical changes leading to irreversible injury without the disadvantages of surgical manipulation required by all previous models of reversible cerebral ischemia.  相似文献   

14.
A new model of temporary focal neocortical ischemia in the rat.   总被引:6,自引:0,他引:6  
BACKGROUND AND PURPOSE: We describe a new rat model of temporary focal ischemia that produces neocortical ischemia without the need for prolonged anesthesia. METHODS: Temporary focal cerebral ischemia was initiated during halothane anesthesia, maintained for varying periods without anesthesia, and reversed by clip removal requiring brief anesthesia. Tandem carotid and middle cerebral artery occlusion for 1-4 hours and permanent occlusion were used to determine the duration and extent of ischemia necessary to produce predictable volumes of neocortical infarction in Wistar and spontaneously hypertensive rats. RESULTS: In Wistar rats, occlusion of the right middle cerebral and both common carotid arteries resulted in cerebral blood flow reductions to approximately 8% of baseline. One hour of transient ischemia with 23 hours of reperfusion did not result in infarction. Three hours of ischemia followed by 21 hours of reperfusion resulted in infarction comparable to that caused by 24 hours of permanent ischemia. In spontaneously hypertensive rats, unilateral right middle cerebral and common carotid artery occlusion reduced cerebral blood flow to approximately 11% of baseline. Minimal damage was seen with 1 hour of reversible ischemia, but intervals of 2 and subsequently 3 hours followed by 22-21 hours of reperfusion produced progressively larger infarcts. Damage indistinguishable from that seen with 24 hours of permanent ischemia was seen with 3 or 4 hours of transient ischemia followed by 21 or 20 hours of reperfusion. CONCLUSIONS: For unanesthetized normothermic rats, cerebral blood flow reductions to 10-20% of baseline resulted in maximal infarction once ischemic durations exceeded 2-3 hours. To be effective, experimental therapies aimed at lessening infarct size or restoring blood flow must be initiated within this critical time interval.  相似文献   

15.
BACKGROUND AND PURPOSE: Stroke in preterm and term babies is common and results in significant morbidity. The vulnerability and pathophysiological mechanisms of neonatal cerebral ischemia-reperfusion may differ from those in the mature cerebral nervous system because of the immaturity of many receptor systems and differences in metabolism in neonatal brain. This study details the neuropathological sequelae of reperfusion-induced brain injury after transient middle cerebral artery (MCA) occlusion in the postnatal day 7 (P7) rat. METHODS: P7 rats were subjected to 3 hours of MCA occlusion followed by reperfusion or sham surgery. Diffusion-weighted MRI was performed during MCA occlusion, and maps of the apparent diffusion coefficient (ADC) were constructed. Contrast-enhanced MRI was performed in a subset of animals before and 20 minutes after reperfusion. Triphenyltetrazolium chloride (TTC) staining of the brain was performed 24 hours after reperfusion. Immunohistochemistry to identify astrocytes (glial fibrillary acidic protein), reactive microglia (ED-1), and neurons (microtubule-associated protein 2) and cresyl violet staining were done 4, 8, 24, and 72 hours after reperfusion. RESULTS: On contrast-enhanced MRI, nearly complete disruption of cerebral blood flow was evident in the vascular territory of the MCA during occlusion. Partial restoration of blood flow occurred after removal of the suture. A significant decrease of the ADC, indicative of early cytotoxic edema, occurred in anatomic regions with a disrupted blood supply. The decline in ADC was associated with TTC- and cresyl violet-determined brain injury in these regions 24 hours later. The ischemic core was rapidly infiltrated with reactive microglia and was surrounded by reactive astroglia. CONCLUSIONS: In P7 rats, transient MCA occlusion causes acute cytotoxic edema and severe unilateral brain injury. The presence of a prominent inflammatory response suggests that both the ischemic episode and the reperfusion contribute to the neuropathological outcome.  相似文献   

16.
目的 确立更规范统一的制作大鼠局灶性脑缺血模型方法,使脑梗死体积更加稳定。方法 对24只大鼠使用液态硅胶涂层尼龙线栓塞大脑中动脉,分别缺血l,2,6和24h后再灌注24h,监测缺血侧局部脑血流,测定脑梗死体积及脑水肿程度。结果 缺血后所有大鼠局部脑血流均降到缺血前基值的25%以下,TTC染色显示所有动物在缺血侧皮质和尾状核均有明显的梗死灶和缺血,缺血1h组梗死体积与缺血2h以上组有显性差异,缺血2h以上各组之间梗死体积无显性差异;各组脑水肿程度无显性差异。结论 应用硅胶涂层尼龙线结合局部脑血流监测,缺血2h以上同时予以血流监测,可制作梗死体积稳定的大鼠局灶性脑缺血模型。  相似文献   

17.
To enhance the consistency of the ischemic insult caused by reversible transorbital middle cerebral artery occlusion, we investigated the variability of somatosensory evoked potential amplitudes and regional cerebral blood flow in 26 anesthetized cats using four procedures to induce transient ischemia. These procedures included 60 minutes of left middle cerebral artery occlusion with or without left common carotid artery occlusion and 120 minutes of left middle cerebral artery occlusion with or without bilateral common carotid artery occlusion. Blood flow in the left middle cerebral artery territory was markedly and consistently reduced to less than 20 ml/min/100 g with simultaneous occlusion of the left middle cerebral artery and both common carotid arteries. The standard deviation of blood flow with this procedure (5.4) was less than that with the other three procedures (13-25). The amplitudes of ipsilateral somatosensory evoked potentials were decreased to approximately 20% of control during ischemia with all four procedures. During reperfusion, amplitudes recovered more slowly, to half of control, after both procedures involving 120 minutes of ischemia. After 120 minutes of reperfusion, the range of amplitudes was smallest in the group exposed to middle cerebral artery occlusion with bilateral common carotid artery occlusion. The degree of recovery of the somatosensory evoked potentials correlated with residual blood flow in both the ipsilateral middle cerebral artery territory and in the white matter during ischemia. We conclude that the most consistent model of focal ischemia and reperfusion in cats in which there is partial recovery of somatosensory evoked potentials is occlusion of one middle cerebral artery and both common carotid arteries for 120 minutes.  相似文献   

18.
目的 探讨消炎痛和美洛昔康对再灌注后脑损伤的影响及作用机制.方法 线栓法制作大鼠大脑中动脉缺血模型(MCAO).用免疫组化方法观察脑组织ICAM-1、E-选择素的表达.白细胞髓过氧化物酶(MPO)检测试剂盒检测MPO活性.用放射免疫方法检测PGE2的浓度.TTC染色观察梗死范围.结果 消炎痛和美洛昔康早期给药,都能减小皮层梗死体积.再灌注后4h给药,对梗死体积都无明显影响.再灌注后缺血侧皮层和纹体PGE2浓度明显升高,MPO活性增高,消炎痛和美洛昔康均能降低皮层和纹体区PGE2的水平,明显减少ICAM-1和E-选择素阳性血管数,降低皮层MPO活性.结论 消炎痛和美洛昔康早期给药能减小皮层的梗死体积,这种脑保护作用与抑制内皮黏附分子的表达,减轻再灌注后炎症反应.随着再灌注时间的延长,这种保护作用减弱.  相似文献   

19.
人工合成E-选择素治疗大鼠局灶脑缺血再灌注损伤的探讨   总被引:2,自引:1,他引:1  
目的:探讨新的药物治疗脑缺血再灌注损伤。方法:用人工合成 E-选择素 2mg·kg-1或 10 mg·kg-1溶解于生理盐水中,静脉注入自发性高血压大鼠永久左侧大脑中动脉/颈总动脉(MCA/CCA)闭塞或MCA/CCA闭塞2h后CCA再灌注模型中。24h后,脑梗死体积用计算机扫描计算。结果:在永久性MCA/CCA闭死组中脑梗死体积没有差别,在MCA/CCA闭死后CCA再灌注组中脑梗死体积有意义地缩小(P<0.01)。结论:E-选择素能够有效地减少大鼠脑缺血再灌注损伤。  相似文献   

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