CENTRAL NERVOUS SYSTEM DYSFUNCTION IN SHOCK AND TRAUMA
休克和创伤中的中枢神经系统功能障碍
基本信息
- 批准号:2177533
- 负责人:
- 金额:$ 24.47万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1988
- 资助国家:美国
- 起止时间:1988-06-01 至 1999-06-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION: (Adapted from the applicant's abstract) The objectives of
the studies are: 1) to elucidate the molecular mechanisms underlying the
role of brain dynorphin/kappa opiate receptor systems in mediating the
CNS response to hypotension; 2) to characterize the temporal and regional
alterations in immediate early gene, stress protein and cytokine
expression in the brain and correlate such changes with gene expression
for opiate peptides and with the cardiovascular and histologic response
to hemorrhage; 3) to characterize the presence and regional activation
of programmed cell death in the brain; and 4) to facilitate the
development of improved molecular and pharmacologic therapeutic
approaches to shock. Preliminary studies have documented that
endogenous opiates, most notably dynorphin, appear to be involved in the
central regulation of cardiovascular function during hemorrhagic shock.
Molecular investigations will continue along this line with selected
areas of brain dysfunction identified. The investigators will examine
the therapeutic efficacy of the k-opioid receptor antagonist, nor-
binaltorphimine, the calcium channel blocker, (s)-emopamil, the IL-1
receptor antagonist, IL1-RA, and the antibody to TNFa alone or in
combination. The studies are to enhance current understanding of the
molecular sequelae of hypotension and low flow states that accompany
shock and trauma so as to foster the development of more effective
pharmacologic and genetic therapeutic approaches to treating shock.
描述:(改编自申请人的摘要)
这些研究是:1)阐明了
脑强啡肽/κ阿片受体系统在介导阿片受体介导
CNS对低血压的反应; 2)表征时间和区域性
即早基因、应激蛋白和细胞因子的改变
并将这些变化与基因表达相关联
以及心血管和组织学反应
出血; 3)表征存在和区域激活
大脑中程序性细胞死亡;以及4)促进
改进的分子和药理学治疗的发展
接近休克。初步研究表明,
内源性阿片类物质,最明显的是强啡肽,似乎参与了
失血性休克时心血管功能的中枢调节
分子研究将继续沿着这条线与选定的
大脑功能障碍的区域。调查人员将检查
K-阿片受体拮抗剂的治疗效果,或-
binaltorphimine,钙通道阻滞剂,(s)-emopamil,IL-1
受体拮抗剂、IL 1-RA和TNF α抗体单独或联合
组合.这些研究是为了加强目前对
伴随低血压和低血流状态的分子后遗症
冲击和创伤,以促进发展更有效的
药理学和基因治疗方法来治疗休克。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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TRACY K. MCINTOSH其他文献
TRACY K. MCINTOSH的其他文献
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{{ truncateString('TRACY K. MCINTOSH', 18)}}的其他基金
NEUROPROTECTIVE GROWTH FACTORS IN TRAUMATIC BRAIN INJURY
创伤性脑损伤中的神经保护生长因子
- 批准号:
6477204 - 财政年份:2000
- 资助金额:
$ 24.47万 - 项目类别:
NEUROPROTECTIVE GROWTH FACTORS IN TRAUMATIC BRAIN INJURY
创伤性脑损伤中的神经保护生长因子
- 批准号:
6625506 - 财政年份:2000
- 资助金额:
$ 24.47万 - 项目类别:
NEUROPROTECTIVE GROWTH FACTORS IN TRAUMATIC BRAIN INJURY
创伤性脑损伤中的神经保护生长因子
- 批准号:
6679479 - 财政年份:2000
- 资助金额:
$ 24.47万 - 项目类别:
NEUROPROTECTIVE GROWTH FACTORS IN TRAUMATIC BRAIN INJURY
创伤性脑损伤中的神经保护生长因子
- 批准号:
6256519 - 财政年份:2000
- 资助金额:
$ 24.47万 - 项目类别:
CENTRAL NERVOUS SYSTEM DYSFUNCTION IN SHOCK AND TRAUMA
休克和创伤中的中枢神经系统功能障碍
- 批准号:
6476457 - 财政年份:1988
- 资助金额:
$ 24.47万 - 项目类别:
MAGNESIUM AND THE PATHOPHYSIOLOGY OF BRAIN INJURY
镁与脑损伤的病理生理学
- 批准号:
2266127 - 财政年份:1988
- 资助金额:
$ 24.47万 - 项目类别:
ENDORPHINS AND CATECHOLAMINES IN SHOCK AND TRAUMA
休克和创伤中的内啡肽和儿茶酚胺
- 批准号:
3286110 - 财政年份:1988
- 资助金额:
$ 24.47万 - 项目类别:
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