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Cerebral ischemia and reperfusion injury: The role of the white blood cell and white blood cell modulation by pentoxifylline.

机译:脑缺血和再灌注损伤:己酮可可碱对白细胞和白细胞的调节作用。

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摘要

Cerebral ischemic and reperfusion injury result form a number of reasons including shock, trauma, cerebral blood clot or cardiac arrest. It results from an inadequate blood supply to the brain which can be further exacerbated during the reperfusion period when blood flow resumes. It is important to understand the mechanisms involved during this process so that therapeutic interventions be directed at reducing the resulting injury.; White blood cells (leukocytes) are competent scavengers of tissue debris and are a vital component of the proinflammatory response generated during ischemia and reperfusion. Their role in this injury process has also been shown to be deleterious as well as beneficial in the heart, skeletal muscle and intestine. Leukocytes may contribute to this increased injury by either physically plugging the vasculature or by the release of chemical mediators which result in increased damage. It was the purpose of this study to determine if white blood cells contribute to the injury which results from ischemia and reperfusion in the brain.; Control and vinblastine-induced leukopenic rats were compared using a model of global forebrain ischemia with reperfusion in the rat. Somatosensory evoked potentials (SSEP), EEG activity, and TTC defined cerebral infarcts were compared as indices of functional cortical damage. In addition, pentoxifylline, a drug shown to increase leukocyte deformability and function was tested along with controls on influencing SSEP and EEG activity following cerebral ischemia and reperfusion.; Results indicate that white blood cells contribute to the injury that results from cerebral ischemia and reperfusion. This was indicated by a preservation of the SSEP and EEG activity as well as a reduction in the cerebral infarct size in the leukopenic rats. The preservation of cortical functional damage also indicated a therapeutic potential for Pentoxifylline along with implicating a white blood cell mechanism for its effect.
机译:脑缺血和再灌注损伤的结果是多种原因引起的,包括休克,创伤,脑血栓或心脏骤停。它是由大脑供血不足导致的,在血液恢复流动的再灌注期间,这种情况可能会进一步恶化。重要的是要了解此过程中涉及的机制,以使治疗性干预措施能够减少造成的伤害。白细胞(白细胞)是组织碎片的有效清除剂,并且是缺血和再灌注过程中产生的促炎反应的重要组成部分。它们在这种损伤过程中的作用也被证明是有害的,并且对心脏,骨骼肌和肠道有益。白细胞可能通过物理堵塞脉管系统或释放化学介质而导致这种增加的损伤,从而导致损伤增加。这项研究的目的是确定白细胞是否是由脑缺血和再灌注导致的损伤。使用大鼠全脑缺血再灌注模型比较对照组和长春碱诱导的白细胞减少症大鼠。将体感诱发电位(SSEP),脑电活动和TTC定义的脑梗死作为功能性皮层损害的指标进行了比较。此外,还对己酮可可碱(一种显示出可增加白细胞变形性和功能的药物)以及对脑缺血和再灌注后影响SSEP和EEG活性的对照进行了测试。结果表明,白细胞对脑缺血和再灌注造成的损伤有贡献。这可以通过保持SSEP和EEG活性以及减少白细胞减少症大鼠的脑梗死面积来表明。皮质功能损伤的保存还表明了己酮可可碱的治疗潜力,并暗示其作用有白细胞机制。

著录项

  • 作者

    Heinel, Lynn Ann.;

  • 作者单位

    Temple University.;

  • 授予单位 Temple University.;
  • 学科 Biology Animal Physiology.
  • 学位 Ph.D.
  • 年度 1992
  • 页码 147 p.
  • 总页数 147
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生理学;
  • 关键词

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