Morphological changes and molecular mechanism in the carotid bodies after the termination of chronic hypoxia

慢性缺氧终止后颈动脉体的形态变化及分子机制

基本信息

  • 批准号:
    13680048
  • 负责人:
  • 金额:
    $ 1.98万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2001
  • 资助国家:
    日本
  • 起止时间:
    2001 至 2002
  • 项目状态:
    已结题

项目摘要

The carotid bodies after 2, 4, and 8 weeks of hypoxic exposure were enlarged by 1.2-1.5 times in the short axis, and 1.3-1.7 times in the long axis in comparison with the normoxic control ones. The enlarged carotid bodies contained a number of expanded vasculatures. Mean density of substance P (SP) and calcitonin gene-related peptide (CGRP) containing fibers was transiently high in the carotid bodies after 4 weeks hypoxic exposure, and decreased in those after 8-12 weeks exposure. Density of vasoactive intestinal polypeptide (VIP) fibers increased significantly in all periods of hypoxic exposure observed, and was especially high in those after 4 weeks exposure. Density of neuropeptide Y fibers was unchanged in the carotid bodies during hypoxic exposure. These characteristic changes suggest a possibility that the role of these neuropeptide containing fibers may be different in the carotid bodies after each of four periods of hypoxic exposureIn the carotid bodies after 8 weeks of hypoxic exposure, the percentage of small vessels with diameters less than 5 μm decreased to under 20%, that of diameters greater than 16 μm increased to over 20%. The carotid bodies 1 and 2 weeks after the termination of chronic hypoxia were diminished in size, although their short and long axes remained larger than the normoxic controls. Those 4 and 8 weeks after the termination of chronic hypoxia were diminished to nearly normoxic control level. In those 8 weeks after the termination of chronic hypoxia, about 45% of the blood vessels were small ones with diameters less than 5 μm and 10 μm. The percentage of relatively large vessels with diameters greater than 16 μm was less than 10%. In the carotid bodies 4 weeks after the termination of hypoxia, the density of NPY fibers increased
缺氧2、4、8周后,颈动脉体短轴增大1.2-1.5倍,长轴增大1.3-1.7倍。增大的颈动脉体含有大量扩张的血管。低氧暴露4周后,颈动脉体内含P物质(SP)和降钙素基因相关肽(CGRP)纤维的平均密度短暂增高,8-12周后降低。血管活性肠多肽(VIP)纤维的密度增加显着在所有观察到的低氧暴露期间,尤其是在那些暴露4周后。在缺氧暴露期间,颈动脉体中的神经肽Y纤维的密度不变。这些特征性的变化提示,在4个低氧暴露期中,这些含神经肽纤维在颈动脉体中的作用可能不同。在低氧暴露8周后的颈动脉体中,直径小于5 μm的小血管所占的百分比下降到20%以下,直径大于16 μm的小血管所占的百分比增加到20%以上。颈动脉体1和2周后终止慢性缺氧的大小减少,虽然他们的短轴和长轴仍然大于常氧对照组。慢性缺氧结束后4周和8周,缺氧大鼠的脑组织已恢复到接近常氧对照组的水平。在慢性缺氧结束后8周,约45%的血管为直径小于5 μm和10 μm的小血管。直径大于16 μm的相对较大血管的百分比小于10%。缺氧结束后4周,颈动脉体内NPY纤维密度增加

项目成果

期刊论文数量(26)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
T.Kusakabe: "The carotid labyrinth of amphibians."Microsc. Res. Tech.. 59. 207-226 (2002)
T.Kusakabe:“两栖动物的颈动脉迷宫。”Microsc。
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    0
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H.Hiruma, et al.: "Neuropeptide Y inhibits axonal transport of particles of adult caltured dorsal ganglion cells."J. Physiol.. 543. 85-97 (2002)
H.Hiruma 等人:“神经肽 Y 抑制成体培养的背神经节细胞颗粒的轴突运输。”J.
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    0
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F,Obata et al.: "Selenium-dependent glutatione peroxidase-GI is localized in basal granulated cells of rat stomach"Biomed. Res.. 22. 7-14 (2001)
F,Obata 等人:“硒依赖性谷胱甘肽过氧化物酶-GI 位于大鼠胃的基底颗粒细胞中”Biomed。
  • DOI:
  • 发表时间:
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  • 影响因子:
    0
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T.Kusakabe, et al.: "Changes in the peptidergic innervation in the carotid body of the rats chronically exposed to hypercapnic hypoxia : an effect of arterial CO2 tension"Histol. Histopathol.. 17. 21-29 (2002)
T.Kusakabe 等人:“长期暴露于高碳酸血症缺氧的大鼠颈动脉体肽能神经支配的变化:动脉 CO2 张力的影响”Histol。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
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日下部 辰三: "低酸素環境下における化学受容機構の研究:現状と今後の問題点."臨床スポーツ医学. 18. 827-829 (2001)
Tatsuzo Kusakabe:“缺氧环境下化学感受器机制的研究:现状和未来问题。” 18. 827-829 (2001)。
  • DOI:
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    0
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KUSAKABE Tatsumi其他文献

KUSAKABE Tatsumi的其他文献

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{{ truncateString('KUSAKABE Tatsumi', 18)}}的其他基金

Basic studies on high-altitude training : Chemoreceptor mechanism on spontaneously hypertensive rats(SHR) in chronic hypoxia
高海拔训练基础研究:慢性缺氧下自发性高血压大鼠(SHR)的化学感受器机制
  • 批准号:
    21500636
  • 财政年份:
    2009
  • 资助金额:
    $ 1.98万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Basic studies on high-altitude training : Changes in the sensitivity on airway mucosa in chronic hypoxia
高海拔训练基础研究:慢性缺氧时气道黏膜敏感性的变化
  • 批准号:
    19500569
  • 财政年份:
    2007
  • 资助金额:
    $ 1.98万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Basic researches on the high altitude training : mechanism of vascular and pulmonary systems
高海拔训练的基础研究:血管和肺系统的机制
  • 批准号:
    17500441
  • 财政年份:
    2005
  • 资助金额:
    $ 1.98万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Three-dimensional analysis and molecular Mechanism of the autonomic nervous system in chronically hypoxic carotid body
颈动脉体慢性缺氧自主神经系统三维分析及分子机制
  • 批准号:
    11670015
  • 财政年份:
    1999
  • 资助金额:
    $ 1.98万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Three-dimensional analysis and molecular mechanism of the peptidergic innervation in the arterial chemoreceptor organ
动脉化学感受器肽能神经支配的三维分析及分子机制
  • 批准号:
    09670022
  • 财政年份:
    1997
  • 资助金额:
    $ 1.98万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular mechanism and ultrastructure of the arterial chemoreceptor organ in chronically hypoxia
慢性缺氧时动脉化学感受器的分子机制及超微结构
  • 批准号:
    05670024
  • 财政年份:
    1993
  • 资助金额:
    $ 1.98万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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NSF PRFB 2023 财年:通过跨代可塑性响应鱼类缺氧的遗传表型和机制
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    2305837
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    2024
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Integrated understanding and manipulation of hypoxic cellular functions by artificial nucleic acids with hypoxia-accumulating properties
具有缺氧累积特性的人工核酸对缺氧细胞功能的综合理解和操纵
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    23H02086
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    2023
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Development of transcatheter arterial embolization for controlling hypoxia in hepatocellular carcinoma
经导管动脉栓塞控制肝细胞癌缺氧的研究进展
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    23K07075
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    2023
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Function, regulation, and conservation of hypoxia-induced glycolysis condensates
缺氧诱导的糖酵解缩合物的功能、调节和保存
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    10552295
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研究缺氧诱导因子-1 (HIF-1) 作为幼年特发性关节炎的新治疗靶点。
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    23K14987
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