Summers Richard L, Martin David S, Meck Janice V, Coleman Thomas G
Department of Emergency Medicine, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
Comput Biol Med. 2007 Mar;37(3):358-63. doi: 10.1016/j.compbiomed.2006.04.003. Epub 2006 Jun 30.
Circulatory adaptations resulting in postflight orthostasis have frequently been observed in response to space travel. It has been postulated that a decrement in left ventricular mass (LVM) found after microgravity exposure may be the central component in this cardiovascular deconditioning. However, a physiologic mechanism responsible for these changes in the myocardium has not been determined. In this study, we examined the sequential alterations in echocardiographic measured LVM from preflight to landing day and 3 days into the postflight recovery period. In a previous study in returning astronauts we found a comparative 9.1% reduction in postflight LVM that returned to preflight values by the third day of recovery. This data was further evaluated in a systems analysis approach using a well-established advanced computer model of circulatory functioning. The computer model incorporates the physiologic responses to changes in pressures, flows and hydraulics within the circulatory system as affected by gravitational forces. Myocardial muscle progression to atrophy or hypertrophy in reaction to the circulatory load conditions is also included in the model. The integrative computer analysis suggests that these variations in LVM could be explained by simple fluid shifts known to occur during spaceflight and can reverse within a few days after reentry into earth's gravity. According to model predictions, the reductions in LVM found upon exposure to microgravity are a result of a contraction of the myocardial interstitial fluid space secondary to a loss in the plasma volume. This hypothesis was additionally supported by the published ground-based study in which we followed the alterations in LVM and plasma volume in normal subjects in which hypovolemia was induced by simple dehydration. In the hypovolemic state, plasma volume was reduced in these subjects and was significantly correlated with echocardiographic measurements of LVM. Based on these experimental findings and the performance of the computer systems analysis it appears that reductions in LVM observed after spaceflight may be secondary to fluid exchanges produced by common physiologic mechanisms. Reductions in LVM observed after microgravity exposure have been previously postulated to be a central component of spaceflight-induced cardiovascular deconditioning. However, a recent study has demonstrated a return of astronauts' LVM to preflight values by the third day after landing through uncertain mechanisms. A systems analysis approach using computer simulation techniques allows for a dissection of the complex physiologic control processes and a more detailed examination of the phenomena. From the simulation studies and computer analysis it appears that microgravity induced reductions in LVM may be explained by considering physiologic fluid exchanges rather than cardiac muscle atrophy.
在太空旅行后，经常会观察到导致飞行后直立性低血压的循环系统适应性变化。据推测，微重力暴露后左心室质量（LVM）的减少可能是这种心血管功能失调的核心因素。然而，导致心肌这些变化的生理机制尚未确定。在本研究中，我们检查了从飞行前到着陆日以及飞行后恢复期第3天通过超声心动图测量的LVM的连续变化。在之前一项针对返回地球的宇航员的研究中，我们发现飞行后LVM相对减少了9.1%，在恢复的第三天恢复到飞行前的值。使用一个成熟的先进循环功能计算机模型，以系统分析方法对这些数据进行了进一步评估。该计算机模型纳入了循环系统内压力、流量和液压变化所产生的生理反应，这些变化受重力影响。模型中还包括心肌对循环负荷条件反应时出现的萎缩或肥大过程。综合计算机分析表明，LVM的这些变化可以用太空飞行期间已知会发生的简单液体转移来解释，并且在重新进入地球重力环境后的几天内可以逆转。根据模型预测，暴露于微重力时LVM的减少是由于血浆量减少导致心肌间质液空间收缩的结果。一项已发表的地面研究进一步支持了这一假设，在该研究中，我们追踪了正常受试者因简单脱水导致血容量不足时LVM和血浆量的变化。在血容量不足状态下，这些受试者的血浆量减少，并且与LVM的超声心动图测量值显著相关。基于这些实验结果以及计算机系统分析的结果，似乎太空飞行后观察到的LVM减少可能是常见生理机制产生的液体交换的继发结果。之前曾推测，微重力暴露后LVM的减少是太空飞行引起的心血管功能失调的核心因素。然而，最近一项研究表明，宇航员的LVM在着陆后第三天通过不确定的机制恢复到飞行前的值。使用计算机模拟技术的系统分析方法能够剖析复杂的生理控制过程，并更详细地研究这些现象。从模拟研究和计算机分析来看，微重力引起的LVM减少似乎可以通过考虑生理液体交换而非心肌萎缩来解释。
