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
- 来源:
- 关键词:
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。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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.
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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
- 作者:
- 通讯作者:
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:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
KUSAKABE Tatsumi其他文献
KUSAKABE Tatsumi的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ 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)
相似海外基金
NSF PRFB FY 2023: Heritable phenotypes and mechanisms through transgenerational plasticity in response to hypoxia in fish
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
- 批准号:
2305837 - 财政年份:2024
- 资助金额:
$ 1.98万 - 项目类别:
Fellowship Award
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
- 批准号:
23H02086 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
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
- 批准号:
23K07075 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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
- 批准号:
10552295 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
NSF-BSF: Mechanism of Cuticle Remodeling by Hypoxia
NSF-BSF:缺氧角质层重塑机制
- 批准号:
2308879 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Continuing Grant
Investigation of hypoxia-inducible factor-1 (HIF-1) as a novel therapeutic target for juvenile idiopathic arthritis.
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。
- 批准号:
23K14987 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Grant-in-Aid for Early-Career Scientists
Dissecting the role of hypoxia in T cell differentiation in cancer
剖析缺氧在癌症 T 细胞分化中的作用
- 批准号:
10578000 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Intermittent Hypoxia Initiated Motor Plasticity in Individuals with Multiple Sclerosis
间歇性缺氧引发多发性硬化症患者的运动可塑性
- 批准号:
10593412 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
NSF/BIO-DFG: Cytochrome c oxidase adaptation to hypoxia in systemic vascular cells - From structure to function
NSF/BIO-DFG:细胞色素 c 氧化酶对全身血管细胞缺氧的适应 - 从结构到功能
- 批准号:
2329629 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Standard Grant
Acute intermittent hypoxia as a novel cardio-therapeutic for spinal cord injury
急性间歇性缺氧作为脊髓损伤的新型心脏治疗方法
- 批准号:
478667 - 财政年份:2023
- 资助金额:
$ 1.98万 - 项目类别:
Operating Grants