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飞行后心血管功能障碍的外周效应器机制假说

Peripheral effector mechanism hypothesis of postflight cardiovascular dysfunction.

作者信息

Zhang L F, Yu Z B, Ma J, Mao Q W

机构信息

Department of Aerospace Physiology, The Fourth Military Medical University, Xi'an, PR China.

出版信息

Aviat Space Environ Med. 2001 Jun;72(6):567-75.

PMID:11396563
Abstract

Studies on the mechanisms of cardiovascular dysfunction after space-flight are important to illustrate the cardiovascular effect of microgravity and develop appropriate multi-system countermeasures for future long-duration spaceflights. Over the past 10 yr, we have systematically studied the adaptational changes in structure and function of both the heart and vessels, using the tail-suspension rat model to simulate microgravity effects. Our results indicate that simulated microgravity induced atrophic changes and reduced contractility of the heart muscle, and upward- and downward-regulation in structure, function, and innervation state of vessels in the brain and hind body of the rat. In addition, more recent advances in relevant ground-based and space-flight studies from different laboratories have also been reviewed. Based on these studies, it has been speculated that, in addition to hypovolemia, the microgravity-induced adaptational changes in the structure and function of the two main effectors of the cardiovascular system, i.e., the arterial smooth muscle and the cardiac muscle, might be among the most important mechanisms responsible for postflight cardiovascular dysfunction and orthostatic intolerance. In this paper we will review the available evidence with comments.

摘要

研究太空飞行后心血管功能障碍的机制,对于阐明微重力对心血管系统的影响以及为未来长期太空飞行制定合适的多系统应对措施具有重要意义。在过去10年中,我们利用尾悬吊大鼠模型模拟微重力效应,系统地研究了心脏和血管结构与功能的适应性变化。我们的研究结果表明,模拟微重力会导致心肌萎缩和收缩力下降,以及大鼠脑部和后躯血管在结构、功能和神经支配状态上的上调和下调。此外,还综述了来自不同实验室的相关地面研究和太空飞行研究的最新进展。基于这些研究,据推测,除血容量减少外,心血管系统的两个主要效应器即动脉平滑肌和心肌在结构和功能上的微重力诱导适应性变化,可能是飞行后心血管功能障碍和体位性不耐受的最重要机制之一。在本文中,我们将对现有证据进行综述并加以评论。

相似文献

1
Peripheral effector mechanism hypothesis of postflight cardiovascular dysfunction.飞行后心血管功能障碍的外周效应器机制假说
Aviat Space Environ Med. 2001 Jun;72(6):567-75.
2
[Peripheral effector mechanism hypothesis on cardiovascular dysfunction after spaceflight].[关于航天飞行后心血管功能障碍的外周效应器机制假说]
Sheng Li Ke Xue Jin Zhan. 2001 Jan;32(1):13-7.
3
Plasticity of arterial vasculature during simulated weightlessness and its possible role in the genesis of postflight orthostatic intolerance.模拟失重状态下动脉血管系统的可塑性及其在飞行后体位性不耐受发生机制中的可能作用。
J Gravit Physiol. 1997 Jul;4(2):P97-100.
4
[Plastic changes of structure, function and perivascular innvervation of arterial vasculature during simulated weightlessness].模拟失重期间动脉血管结构、功能及血管周围神经支配的可塑性变化
Space Med Med Eng (Beijing). 1998 Jun;11(3):215-9.
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Cardiovascular peripheral effector mechanism in postflight orthostatic intolerance: a simulation study.飞行后体位性不耐受的心血管外周效应机制:一项模拟研究
J Gravit Physiol. 2000 Jul;7(2):P151-2.
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[Effects of simulated microgravity on cardiovascular function and counter effect of lower body negative pressure].[模拟微重力对心血管功能的影响及下体负压的对抗作用]
Space Med Med Eng (Beijing). 2002 Aug;15(4):235-40.
7
[A simulation study of effects of depressed myocardial contractility on cardiovascular response to lower body negative pressure].[心肌收缩力降低对下体负压心血管反应影响的模拟研究]
Space Med Med Eng (Beijing). 2001 Aug;14(4):253-6.
8
Insight into mechanisms of reduced orthostatic performance after exposure to microgravity: comparison of ground-based and space flight data.深入了解暴露于微重力环境后立位耐力降低的机制:地面和太空飞行数据的比较
J Gravit Physiol. 1998 Jul;5(1):P85-8.
9
Vasoconstrictor responsiveness of hind body vascular beds is diminished in tail-suspended rats.尾部悬吊大鼠后体血管床的血管收缩反应性降低。
J Gravit Physiol. 2000 Jul;7(2):P153-4.
10
[The changes of cardiovascular response to orthostatic stress caused by hypovolemia induced by weightlessness: a simulation study].[失重诱导的低血容量对直立位应激心血管反应的影响:一项模拟研究]
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2002 Jan;19(1):48-52.

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