Vernice Nicholas A, Meydan Cem, Afshinnekoo Ebrahim, Mason Christopher E
The Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Weill Cornell Medicine, 1305 York Avenue, New York, NY 10021, USA.
Precis Clin Med. 2020 Dec;3(4):284-291. doi: 10.1093/pcmedi/pbaa022. Epub 2020 Jun 16.
While early investigations into the physiological effects of spaceflight suggest the body's ability to reversibly adapt, the corresponding effects of long-term spaceflight (>6 months) are much less conclusive. Prolonged exposure to microgravity and radiation yields profound effects on the cardiovascular system, including a massive cephalad fluid translocation and altered arterial pressure, which attenuate blood pressure regulatory mechanisms and increase cardiac output. Also, central venous pressure decreases as a result of the loss of venous compression. The stimulation of baroreceptors by the cephalad shift results in an approximately 10%-15% reduction in plasma volume, with fluid translocating from the vascular lumen to the interstitium. Despite possible increases in cardiac workload, myocyte atrophy and notable, yet unexplained, alterations in hematocrit have been observed. Atrophy is postulated to result from shunting of protein synthesis from the endoplasmic reticulum to the mitochondria via mortalin-mediated action. While data are scarce regarding their causative agents, arrhythmias have been frequently reported, albeit sublethal, during both Russian and American expeditions, with QT interval prolongation observed in long, but not short duration, spaceflight. Exposure of the heart to the proton and heavy ion radiation of deep space has also been shown to result in coronary artery degeneration, aortic stiffness, carotid intima thickening via collagen-mediated action, accelerated atherosclerosis, and induction of a pro-inflammatory state. Upon return, long-term spaceflight frequently results in orthostatic intolerance and altered sympathetic responses, which can prove hazardous should any rapid mobilization or evacuation be required, and indicates that these cardiac risks should be especially monitored for future missions.
虽然早期对太空飞行生理效应的研究表明身体有能力进行可逆性适应，但长期太空飞行（>6个月）的相应影响却远没有那么确凿。长时间暴露于微重力和辐射会对心血管系统产生深远影响，包括大量的头向体液转移和动脉压改变，这会削弱血压调节机制并增加心输出量。此外，由于静脉压迫的丧失，中心静脉压会降低。头向移位对压力感受器的刺激导致血浆量减少约10%-15%，液体从血管腔转移到间质。尽管心脏工作量可能增加，但已观察到心肌细胞萎缩以及血细胞比容出现显著但原因不明的变化。据推测，萎缩是由于蛋白质合成通过mortalin介导的作用从内质网转移到线粒体所致。虽然关于心律失常的致病因素数据稀少，但在俄罗斯和美国的太空任务中都经常报告心律失常，尽管是亚致死性的，在长时间而非短时间的太空飞行中观察到QT间期延长。心脏暴露于深空的质子和重离子辐射也已被证明会导致冠状动脉退化、主动脉僵硬、通过胶原介导的作用使颈动脉内膜增厚、加速动脉粥样硬化以及引发促炎状态。返回后，长期太空飞行经常会导致体位性不耐受和交感反应改变，如果需要任何快速行动或撤离，这可能会很危险，这表明在未来任务中应特别监测这些心脏风险。
