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71.
缺血预处理对缺血再灌注后兔脊髓磷酸腺苷代谢的影响 总被引:5,自引:0,他引:5
目的:研究缺血参处理对缺血再灌注后兔脊髓磷酸腺苷代谢的影响。方法:往置入腹主动脉的Swan-Ganz导管气囊内注气造成兔腰髓缺血模型。将实验兔分为假手术组、缺血组和预处理组。应用反相高效液相色谱方法(reverse phase HPLC),对缺血再灌注后不同时间点腰髓组织中磷酸腺苷(ATP、ADP、AMP)的含量进行检测。结果:和假手术组相比,缺血组兔再灌后各时间点腰髓组织ATP含量有明显下降(P<0.01)。与缺血组相应时间点相比,预处理组兔再灌注后腰髓组织ATP含量明显提高(P<0.01)。结论:缺血预处理显著提高缺血再灌注后兔脊髓组织ATP含量,这可能是缺血预处理对脊髓缺血再灌注损伤产生保护作用的机制之一。 相似文献
72.
采用蒙古沙土双侧颈总动脉阻断前脑缺血模型,以放射自显影(反向磷酸化,back-phosphorylation)及免疫印迹(Western blotting)法体外测定缺血时纹状体DARPP-32磷酸化水平和蛋白含量的变化,结果表明,短暂性缺血纹状体DARPP-32的免疫学活性和蛋白含量地明显改变。在缺血10min内,随缺血时间的延长,体外DARPP-32的[^32P]的掺入量在缺血5min时升高,在缺血2,7,10min时均降低,而反向磷酸化的测定结果表明体内DARPP-32磷酸化水平增高,说明缺血可诱导DARPP-32磷酸化水平变化。 相似文献
73.
目的:探讨地高辛抗血清对大鼠实验性心肌缺血/再灌注损伤(MI/R)的心肌氧化应激的影响。方法:采用左冠状动脉前降支结扎30min,复灌45min建立在体大鼠MI/R模型。SD大鼠随机分成假手术组、缺血/再灌注模型组、生理盐水组、维拉帕米组、小、中、大剂量地高辛抗血清组:于再灌注45min后检测左室心尖部缺血区心肌中内洋地黄素含量、心肌细胞膜Na^+,K^+-ATP酶和SOD活性以及MDA含量,光镜下观察心肌组织形态学变化。结果:MI/R组和生理盐水组大鼠心肌组织内洋地黄素水平明显升高,细胞膜Na^+,K^+-ATP酶活性明显下降,心肌组织SOD活性降低,MDA水平升高。治疗组包括维拉帕米组均能减轻心肌组织结构损伤,降低MDA水平,部分恢复SOD活性;但只有地高辛抗血清能降低心肌组织内洋地黄素水平,恢复心肌细胞膜Na^+,K^+-ATP酶活性。结论:地高辛抗血清通过拮抗内洋地黄素,恢复心肌细胞膜Na^+,K^+-ATP酶活性,从而减轻缺血/再灌注时的氧自由基损伤。 相似文献
74.
Márcia Camargo-De-Morais Marta De Freitas Angela G. De Mattos Nádia Schröder Ana C. Zilles Carla S. F. Lisboa Nice Arteni Armando Barlem Rejane Schierholt Guilherme Zwetsch Carlos A. B. Souza Regina Pessoa-Pureur Carlos A. Netto 《Neurochemical research》1996,21(5):595-602
Neurofilaments subunits (NF-H, NF-M, NF-L) and glial fibrillary acidic protein (GFAP) were investigated in the hippocampus
of rats after distinct periods of reperfusion (1 to 15 days) following 20 min of transient global forebrain ischemia in the
rat. In vitro [14Ca]leucine incorporation was not altered until 48 h after the ischemic insult, however concentration of intermediate filament
subunits significantly decreased in this period. Three days after the insult, leucine incorporation significantly increased
while the concentration NF-H, NF-M, and NF-L were still diminished after 15 days of reperfusion. In vitro incorporation of32P into NF-M and NF-L suffered immediately after ischemia, but returned to control values after two days of reperfusion. GFAP
levels decreased immediately after ischemia but quickly recovered and significantly peaked from 7 to 10 days after the insult.
These results suggest that transient ischemia followed by reperfusion causes proteolysis of intermediate filaments in the
hippocampus, and that proteolysis could be facilitated by diminished phosphorylation levels of NF-M and NF-L. 相似文献
75.
目的:探讨彩色多普勒超声技术测量椎动脉血流量对后循环缺血(PCI)的诊断价值。方法:选取2012年1月至2013年1月在本院神经内科住院并接受治疗的PCI患者58例作为观察组,另选取同期住院并确诊为非后循环缺血症的患者50例作为对照组。所有患者均接受颈部血管超声检查,测量椎动脉内径及血流量,观察组患者需行头颅CTA检查,比较两组患者的椎动脉内径、血流量及颈动脉硬化斑块发生率等。结果:观察组患者的椎动脉内径及血流量明显低于对照组,两组比较差异有统计学意义(P〈0.01);观察组颈动脉硬化斑块的发生率为77.5%(44例),对照组颈动脉硬化斑块的发生率为42%(21例),两组比较差异有统计学意义(P〈0.05)。无狭窄、轻度狭窄、重度狭窄及闭塞的椎动脉血流量的变化(此处所指的血流量是指小于200mL/min那部分患者)有明显差异(P〈0.05)。结论:与头颅CTA对比检查,彩色多普勒具有直接、准确、方便及可重复性等优点,可有效的诊断后循环缺血症状。 相似文献
76.
Robert A. Mueller Thomas J. McCown Ricky D. Hunt Cecilia Lundberg George R. Breese 《Cellular and molecular neurobiology》1990,10(3):327-336
1. | Rats which survived hypoglycemia by insulin, hypoxia by 10% O2, or ischemia by carotid ligation and hypotension to 40 mm Hg, evidenced no changes in cerebrospinal fluid (CSF) uridine. Animals which died soon after the above interventions or as a result of KCl-induced cardiac arrest had elevated CSF uridine concentrations. |
2. | Injection of whole blood or the soluble contents of lysed blood cells into the lateral ventricle of rats reduced CSF uridine to less than one-half normal at 24 hrs but values returned to normal 3 days later. Changes in hypoxanthine resembled those of uridine, but were less dramatic, whereas xanthine concentrations were largely unaltered. Intraventricular injection of plasma or saline did not alter CSF uridine. |
3. | It seems most likely that low CSF uridine concentrations previously reported in head injury patients may be secondary to the effects of blood cell contents in the cerebrospinal fluid, rather than responses to altered metabolism in neurons or glia cells. |
77.
Panagiotis Bargiotas Antje Krenz Hannah Monyer Markus Schwaninger 《Channels (Austin, Tex.)》2012,6(6):453-456
Pannexin (Px, Panx) channels have been implicated in several physiological and pathological processes. We recently studied the potential contribution of pannexins in ischemic brain damage using Px1-/- Px2-/- mice and provided evidence that (1) the release of IL-1β and hemichannel function in astrocytes are, in contrast to published data, not affected by the absence of Px1 and Px2, (2) channel function in neurons lacking Px1 and Px2 is impaired and (3) Px1-/- Px2-/- mice had a better functional outcome and smaller infarcts than wild-type mice when subjected to ischemic stroke. Here, we further investigate the neurological outcome of wild-type and pannexin double-knockout mice 48 h after permanent occlusion of the distal middle cerebral artery (MCAO). Pannexin double-knockout mice (Px1-/- Px2-/-) were less impaired in parameters such as exploration, anxiety, sensorimotor function and behavioral symmetry. 相似文献
78.
Yves Harder Daniel Schmauss Reto Wettstein José T. Ega?a Fabian Weiss Andrea Weinzierl Anna Schuldt Hans-Günther Machens Michael D. Menger Farid Rezaeian 《Journal of visualized experiments : JoVE》2014,(93)
Despite profound expertise and advanced surgical techniques, ischemia-induced complications ranging from wound breakdown to extensive tissue necrosis are still occurring, particularly in reconstructive flap surgery. Multiple experimental flap models have been developed to analyze underlying causes and mechanisms and to investigate treatment strategies to prevent ischemic complications. The limiting factor of most models is the lacking possibility to directly and repetitively visualize microvascular architecture and hemodynamics. The goal of the protocol was to present a well-established mouse model affiliating these before mentioned lacking elements. Harder et al. have developed a model of a musculocutaneous flap with a random perfusion pattern that undergoes acute persistent ischemia and results in ~50% necrosis after 10 days if kept untreated. With the aid of intravital epi-fluorescence microscopy, this chamber model allows repetitive visualization of morphology and hemodynamics in different regions of interest over time. Associated processes such as apoptosis, inflammation, microvascular leakage and angiogenesis can be investigated and correlated to immunohistochemical and molecular protein assays. To date, the model has proven feasibility and reproducibility in several published experimental studies investigating the effect of pre-, peri- and postconditioning of ischemically challenged tissue. 相似文献
79.
Jinshan Yang Xiang Luo Xiaojiang Huang Qin Ning Minjie Xie Wei Wang 《Journal of neurochemistry》2014,131(3):383-394
Increasing evidence indicates that the Eph receptors and their ephrin ligands are involved in the regulation of interactions between neurons and astrocytes. Moreover, astrocytic ephrin‐A3 reverse signaling mediated by EphA4 receptors is necessary for controlling the abundance of glial glutamate transporters. However, the role of ephrin‐A3 reverse signaling in astrocytic function and neuronal death under ischemic conditions remains unclear. In the present study, we found that the EphA4 receptor and its ephrin‐A3 ligand, which were distributed in neurons and astrocytes, respectively, in the hippocampus showed a coincident up‐regulation of protein expression in the early stage of ischemia. Application of clustered EphA4 decreased the expressions of astrocytic glutamate transporters together with astrocytic glutamate uptake capacity through activating ephrin‐A3 reverse signaling. In consequence, neuronal loss was aggravated in the CA1 region of the hippocampus accompanied by impaired hippocampus‐dependent spatial memory when clustered EphA4 treatment was administered prior to transient global ischemia. These findings indicate that EphA4‐mediated ephrin‐A3 reverse signaling is a crucial mechanism for astrocytes to control glial glutamate transporters and prevent glutamate excitotoxicity under pathological conditions.
80.
目的:探讨巨噬细胞在大鼠肾脏缺血/再灌注损伤过程中的亚型转变及意义。方法:将30只雄性SD大鼠随机分成假手术组(Sham,n=6)和缺血/再灌组(IRI,夹闭肾动脉45 min,n=24)。IRI组分别于术后0、6、24和72 h取肾组织,每个时相组6只大鼠。用HE染色观察肾组织损伤程度;免疫组化染色检测细胞增殖核抗原(PCNA)的表达;实时定量RT-PCR检测巨噬细胞移动抑制因子(MIF) mRNA的表达;免疫组织荧光染色检测MIF、单核巨噬细胞趋化蛋白-1(MCP-1)以及活化巨噬细胞标志物CD68的表达,流式细胞分析检测巨噬细胞M1和M2亚型的分布特征。结果:病理结果显示大鼠肾局部损伤情况和炎症细胞浸润程度在24 h时最为严重,之后逐渐恢复。PCNA在再灌后表达明显增加,6 h达峰值,72 h表达下降。相比于正常组,再灌组大鼠肾组织中MIF的mRNA和蛋白表达明显升高;MCP-1表达则在6 h达峰值,随后下降;而CD68阳性的巨噬细胞数量明显增加,24 h达峰值,72 h表达下降。更进一步研究发现缺血/再灌注6 h时,M1亚型分布达最高值;之后随着缺血/再灌注时间延长,M1亚群相对含量开始下调,M2随之升高。结论:在肾脏缺血/再灌注早期,M1巨噬细胞介导的组织损伤发挥主要作用,随后M2型表达逐渐上调,并通过促进细胞增殖修复肾组织损伤。 相似文献