首页> 外文会议>European Symposium on Life Sciences in Space >COMPOUND MECHANISM HYPOTHESIS ON +Gz-INDUCED BRAIN INJURY AND DYSFUNCTION OF LEARNING AND MEMORY
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COMPOUND MECHANISM HYPOTHESIS ON +Gz-INDUCED BRAIN INJURY AND DYSFUNCTION OF LEARNING AND MEMORY

机译:复合机制假设对+ GZ诱导的脑损伤和学习记忆功能障碍

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We systematically studied the effect of high-sustained +Gz on the brain and its mechanism in past ten years by animal centrifuge experiments. On the basis of the facts we observed and the more recent advances in acceleration physiology, we put forward a compound mechanism hypothesis to offer a possible explanation for +Gz-induced brain injury and dysfunction of learning and memory. It states that, ischemia during high G exposure might be the main factor accounting for +Gz-induced brain injury and dysfunction of learning and memory, including transient depression of brain energy metabolism, disturbance of ion homeostasis, increased blood-brain barrier permeability, increased brain nitric oxide synthase expression, and the protective effect of heat shock protein 70. In addition, the large rapid change of intracranial pressure and increased stress during +Gz exposure, and the hemorrheologic change after +Gz exposure might be one of the important factors accounting for +Gz-induced brain injury and dysfunction of learning and memory. Modern high performance aircraft is capable of reaching accelerations as high as +9Gz sustained for 15-45s that may exceed the human physiological tolerance. It is well known that +Gz-induced loss of consciousness (G-LOC) that is the main threat for pilots is classically attributed to a decrease in cerebral blood flow that results from a drastic decrease in cerebral perfusion pressure. In addition, a causal relationship might exist between G-LOC and increased stress. Centrifuge training developed in many countries is considered as an appropriate method for preventing G-LOC. The benefits of centrifuge training are an increased G-tolerance resulting from improved skill in performing an anti-G straining maneuver and a better understanding of physiologic mechanisms of G-stress and G-tolerance. However, does repeated G-LOC cause the organic mental syndrome? Are the effects of these exposures additive? We know little about the potential pathophysiological effects of repeated high +Gz exposures on the brain.
机译:我们系统地研究高持续+ GZ对大脑和动物实验离心机其过去十年中的作用机制。在我们所观察到的事实和最近的加速度生理的研究进展的基础上,我们提出了复合机制假说提供了+ GZ-致脑损伤和学习记忆障碍的一个可能的解释。它指出,高G曝光期间缺血可能是正加速度引起的脑损伤和学习与记忆,包括脑能量代谢的瞬态抑郁,离子稳态的紊乱的功能障碍的主要因素会计,增加的血脑屏障通透性,增加脑一氧化氮合成酶的表达,和热休克蛋白70的保护作用另外,+ Gz暴露期间颅内压的大迅速变化和增加的压力,和+ Gz暴露后血液流变学变化可能是占的重要因素之一为+ GZ-致脑损伤和学习记忆功能障碍。现代高性能飞机能够到达的加速度高达+ 9Gz持续15-45s可能超过人体生理耐受。它公知的是+ GZ诱导的意识(G-LOC)的损失是用于导频的主要威胁是经典归因于脑血流的降低,从在脑灌注压的急剧下降的结果。此外,因果关系可能G-LOC和增加的压力之间存在。在许多国家制定离心机训练被认为是防止G-LOC的适当方法。离心机训练的好处是增加从改进技术在执行抗荷动作导致G公差和更好地了解G-压力和G公差的生理机制。然而,不重复的G-LOC原因的器质性精神综合症?难道这些风险添加剂的效果?我们知之甚少的大脑反复高+ Gz暴露的潜在病理生理的影响。

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