Kimzey S L, Leonard J I, Johnson P C
NASA-L.B. Johnson Space Center, General Electric Co. and Baylor College of Medicine, Houston, TX 77058, USA.
Acta Astronaut. 1979 Oct;6(10):1289-303. doi: 10.1016/0094-5765(79)90121-8.
Two ground-based methods of weightlessness simulation--a computer model of erythropoiesis feedback regulation and bedrest--were used to investigate the mechanisms which lead to loss of red cell mass during spaceflight. Both methods were used to simulate the first Skylab mission of 28 days. Human bedrest subjects lose red cell mass linearly with time and in this study the loss was 6.7% at the end of four weeks (compared to 14% in Skylab). Postbedrest recovery of red cell mass was delayed for two weeks during which time a further decline in this quantity was noted. This is consistent with the first Skylab mission but not with the two longer flights of two and three months. Hemoconcentration, observed early in the study, was essentially maintained despite red cell loss because of continued loss of plasma volume. The computer model, using the time-varying hematocrit data to estimate red cell production rates, predicted dynamic behavior of plasma volume and red cell mass that was in close agreement with the measured values. The results support the hypothesis that red cell loss during supine bedrest is a normal physiological feedback process in response to hemoconcentration enhanced tissue oxygenation and suppression of red cell production. In contrast, the delayed postbedrest recovery of red cell mass was more difficult to explain, especially in the light of enhanced reticulocyte indices observed at the onset on ambulation. Model simulation suggested the possibilities, still to be experimentally demonstrated, that this period was marked by some combination of increased oxygen-hemoglobin affinity, small reductions in mean red cell life span, ineffective erythropoiesis, or abnormal reticulocytosis. The question of whether hemoconcentration is the sole contributor to spaceflight red cell losses also remains to be resolved.
采用两种地面模拟失重方法——红细胞生成反馈调节的计算机模型和卧床休息，来研究太空飞行期间导致红细胞量减少的机制。两种方法均用于模拟28天的首次天空实验室任务。卧床休息的人体受试者的红细胞量随时间呈线性减少，在本研究中，四周结束时减少了6.7%（相比之下，天空实验室任务中为14%）。卧床休息后红细胞量的恢复延迟了两周，在此期间，该指标进一步下降。这与首次天空实验室任务一致，但与两次为期两个月和三个月的更长时间飞行情况不符。尽管红细胞减少，但由于血浆量持续减少，在研究早期观察到的血液浓缩基本维持。该计算机模型利用随时间变化的血细胞比容数据来估计红细胞生成率，预测的血浆量和红细胞量的动态行为与测量值密切一致。这些结果支持了这样一种假说，即仰卧卧床休息期间红细胞减少是对血液浓缩、组织氧合增强和红细胞生成受抑制的一种正常生理反馈过程。相比之下，卧床休息后红细胞量恢复延迟则更难解释，尤其是考虑到开始行走时观察到的网织红细胞指数升高。模型模拟提出了一些可能性，仍有待实验验证，即这一时期的特征可能是氧合血红蛋白亲和力增加、平均红细胞寿命略有缩短、无效红细胞生成或异常网织红细胞增多等多种因素的某种组合。血液浓缩是否是太空飞行中红细胞损失的唯一原因这一问题也有待解决。
