Norsk Peter, Asmar Ali, Damgaard Morten, Christensen Niels Juel
J Physiol. 2015 Feb 1;593(3):573-84. doi: 10.1113/jphysiol.2014.284869.
Weightlessness in space induces initially an increase in stroke volume and cardiac output, accompanied by unchanged or slightly reduced blood pressure.It is unclear whether these changes persist throughout months of flight.Here, we show that cardiac output and stroke volume increase by 35–41% between 3 and 6 months on the International Space Station, which is more than during shorter flights.Twenty-four hour ambulatory brachial blood pressure is reduced by 8–10 mmHg by a decrease in systemic vascular resistance of 39%, which is not a result of the suppression of sympathetic nervous activity, and the nightly dip is maintained in space.It remains a challenge to explore what causes the systemic vasodilatation leading to a reduction in blood pressure in space, and whether the unexpectedly high stroke volume and cardiac output can explain some vision acuity problems encountered by astronauts on the International Space Station.
Acute weightlessness in space induces a fluid shift leading to central volume expansion. Simultaneously, blood pressure is either unchanged or decreased slightly. Whether these effects persist for months in space is unclear. Twenty-four hour ambulatory brachial arterial pressures were automatically recorded at 1–2 h intervals with portable equipment in eight male astronauts: once before launch, once between 85 and 192 days in space on the International Space Station and, finally, once at least 2 months after flight. During the same 24 h, cardiac output (rebreathing method) was measured two to five times (on the ground seated), and venous blood was sampled once (also seated on the ground) for determination of plasma catecholamine concentrations. The 24 h average systolic, diastolic and mean arterial pressures (mean ± se) in space were reduced by 8 ± 2 mmHg (P = 0.01; ANOVA), 9 ± 2 mmHg (P < 0.001) and 10 ± 3 mmHg (P = 0.006), respectively. The nightly blood pressure dip of 8 ± 3 mmHg (P = 0.015) was maintained. Cardiac stroke volume and output increased by 35 ± 10% and 41 ± 9% (P < 0.001); heart rate and catecholamine concentrations were unchanged; and systemic vascular resistance was reduced by 39 ± 4% (P < 0.001). The increase in cardiac stroke volume and output is more than previously observed during short duration flights and might be a precipitator for some of the vision problems encountered by the astronauts. The spaceflight vasodilatation mechanism needs to be explored further.
太空失重最初会导致每搏输出量和心输出量增加,同时血压不变或略有下降。目前尚不清楚这些变化是否会在数月的飞行中持续存在。在此,我们表明,在国际空间站上飞行3至6个月期间,心输出量和每搏输出量增加了35%-41%,这比短时间飞行时增加得更多。24小时动态臂血压因全身血管阻力降低39%而降低了8-10 mmHg,这并非交感神经活动受抑制的结果,且夜间血压下降现象在太空中依然存在。探究导致太空血压降低的全身血管舒张的原因,以及意外增高的每搏输出量和心输出量是否能够解释国际空间站上宇航员遇到的一些视力问题,仍然是一项挑战。
太空急性失重会导致体液转移,进而引起中心血容量扩张。与此同时,血压要么不变,要么略有下降。目前尚不清楚这些影响在太空中是否会持续数月。使用便携式设备每隔1-2小时自动记录8名男性宇航员的24小时动态肱动脉血压:一次在发射前,一次在国际空间站飞行85至192天期间,最后一次在飞行至少2个月后。在同一24小时内,测量心输出量(重复呼吸法)两到五次(在地面坐着时测量),并采集一次静脉血(同样在地面坐着时采集)以测定血浆儿茶酚胺浓度。在太空中,24小时平均收缩压、舒张压和平均动脉压(均值±标准误)分别降低了8±2 mmHg(P = 0.01;方差分析)、9±2 mmHg(P < 0.001)和10±3 mmHg(P = 0.006)。夜间血压下降8±3 mmHg(P = 0.015)的现象依然存在。每搏输出量和心输出量分别增加了35±10%和41±9%(P < 0.001);心率和儿茶酚胺浓度未变;全身血管阻力降低了39±4%(P < 0.001)。每搏输出量和心输出量的增加幅度超过了之前在短期飞行中观察到的幅度,可能是宇航员遇到的一些视力问题的诱因。太空飞行血管舒张机制需要进一步探索。