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Neurovascular Injury in Acute Hyperglycemia and Diabetes: a Comparative Analysis in Experimental Stroke

机译:急性高血糖和糖尿病患者的神经血管损伤:实验性卒中的比较分析

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摘要

Admission hyperglycemia impacts ischemic stroke deleteriously, but the relative role of acute hyperglycemia (HG) vs diabetes in the pathogenesis of this poor outcome is not clear. The study aims to determine the effect of acute HG on neurovascular outcomes of stroke under control and diabetic conditions. Moderate acute HG (140–200 mg/dl) was achieved by glucose injection before middle cerebral artery occlusion (MCAO) in control Wistar and diabetic Goto-Kakizaki rats. Following 3 h MCAO/21 h reperfusion, we measured infarct size, hemorrhagic transformation (HT) frequency, excess hemoglobin, neurobehavioral outcome, and MCA matrix metalloprotease activity. Infarct size was significantly smaller in diabetic rats. Moderate acute HG increased neuronal damage in diabetic but not in control rats. HT frequency and hemoglobin were significantly higher in diabetic rats. HG augmented vascular damage in control rats and had no additional effect on bleeding in diabetic rats. Neurological deficit was greater in diabetic rats and was worsened by HG. The finding that functional outcome is poorer in both acute HG and diabetes without a significant increase in infarct size suggests that amplified vascular damage contributes to neurological deficit in hyperglycemia. These results highlight the importance of vascular protection to improve neurological outcome in acute ischemic stroke.
机译:入院高血糖对缺血性卒中具有有害影响,但是尚不清楚急性高血糖(HG)与糖尿病在这种不良预后的发病机理中的相对作用。这项研究旨在确定在控制和糖尿病情况下急性HG对中风神经血管结局的影响。在对照组Wistar和糖尿病Goto-Kakizaki大鼠中,在大脑中动脉阻塞(MCAO)之前,通过葡萄糖注射达到了中等程度的急性HG(140-200 mg / dl)。在3个小时的MCAO / 21个小时的再灌注后,我们测量了梗塞面积,出血转化(HT)频率,血红蛋白过量,神经行为预后以及MCA基质金属蛋白酶活性。糖尿病大鼠的梗塞面积明显较小。中度急性HG增加了糖尿病大鼠的神经元损伤,但对照组没有。糖尿病大鼠的HT频率和血红蛋白显着升高。 HG会增加对照组大鼠的血管损伤,并且对糖尿病大鼠的出血没有其他影响。糖尿病大鼠的神经功能缺损更大,而HG使神经功能缺损恶化。急性HG和糖尿病患者的功能预后均较差,而梗塞面积却没有明显增加,这一发现表明,放大的血管损伤会导致高血糖症的神经功能缺损。这些结果凸显了在急性缺血性卒中中血管保护对改善神经系统预后的重要性。

著录项

  • 来源
    《Translational Stroke Research》 |2011年第3期|391-398|共8页
  • 作者单位

    Program in Clinical and Experimental Therapeutics Department of Clinical and Administrative Pharmacy College of Pharmacy University of Georgia HM-1200 Augusta GA 30912 USA;

    Department of Physiology Georgia Health Sciences University 1120 15th St CA2094 Augusta GA 30912 USA;

    Department of Physiology Georgia Health Sciences University 1120 15th St CA2094 Augusta GA 30912 USA;

    Department of Physiology Georgia Health Sciences University 1120 15th St CA2094 Augusta GA 30912 USA;

    Program in Clinical and Experimental Therapeutics Department of Clinical and Administrative Pharmacy College of Pharmacy University of Georgia HM-1200 Augusta GA 30912 USA;

    Department of Biostatistics Georgia Health Sciences University 1120 15th St CA2094 Augusta GA 30912 USA;

    Department of Neurology Georgia Health Sciences University 1120 15th St CA2094 Augusta GA 30912 USA;

    Program in Clinical and Experimental Therapeutics Department of Clinical and Administrative Pharmacy College of Pharmacy University of Georgia HM-1200 Augusta GA 30912 USA;

    Program in Clinical and Experimental Therapeutics Department of Clinical and Administrative Pharmacy College of Pharmacy University of Georgia HM-1200 Augusta GA 30912 USA;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    MMP-9 metalloproteinase; Minocycline; Cerebral hemorrhage; Ischemia–reperfusion Injury; Type 2 diabetes mellitus; Hyperglycemia;

    机译:MMP-9金属蛋白酶;米诺环素;脑出血;缺血再灌注损伤;2型糖尿病;高血糖;

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