Strollo F, Norsk P, Roecker L, Strollo G, Morè M, Bollanti L, Riondino G, Scano A
Italian National Research Centers on Ageing, Endocrine Unit, Rome, Italy.
Aviat Space Environ Med. 1998 Aug;69(8):777-80.
Microgravity causes cephalad fluid shift and compensatory mechanisms. Hormonal changes suggestive of peripheral sympathetic (catecholaminergic) nervous system activation have been recently found in astronauts during flight. Simulation studies showed increased perivascular sympathetic fiber density in the rat brain.
Intracranial microcirculatory adaptations might also occur in astronauts, involving an increase in the turnover rate of catecholamines, i.e., norepinephrine (NE) and its precursor, Dopamine (DA). DA is known to inhibit prolactin (PRL) release and to enhance growth hormone (GH) secretion by the pituitary. Therefore, increased brain dopaminergic activity would result into lower circulating PRL concentrations. At the same time, plasma levels of GH and of its effector insulin-like growth factor-1 (IGF-1) would increase during flight.
Circulating cortisol (CS), PRL, GH and IGF-1 levels were measured 2 d preflight, inflight (4-5 d after launch) and on different days postflight in four astronauts involved in the Spacelab D-2 mission.
No significant changes were found in CS concentrations. PRL decreased while GH and IGF-1 increased inflight (p < 0.05). After flight no statistically relevant hormonal changes were found with respect to preflight.
The observed hormonal changes were consistent with the original hypothesis that spaceflight might activate CNS adrenergic pathways. They occurred in the absence of two typical markers of stress, namely CS and PRL increase, thus ruling out any non-specific effect of acute stress on the results. In agreement with the most recent results of real and simulated microgravity studies performed in both the experimental animal and in man, these data lend support to the hypothesis that the CNS adrenergic pathways are also activated in the human during spaceflight.
微重力会导致头向体液转移及代偿机制。最近在飞行中的宇航员身上发现了提示外周交感（儿茶酚胺能）神经系统激活的激素变化。模拟研究显示大鼠脑内血管周围交感神经纤维密度增加。
宇航员颅内微循环也可能发生适应性变化，包括儿茶酚胺（即去甲肾上腺素（NE）及其前体多巴胺（DA））周转率增加。已知DA可抑制催乳素（PRL）释放，并增强垂体生长激素（GH）分泌。因此，脑内多巴胺能活性增加会导致循环PRL浓度降低。同时，飞行期间GH及其效应物胰岛素样生长因子-1（IGF-1）的血浆水平会升高。
在参与太空实验室D-2任务的四名宇航员中，于飞行前2天、飞行中（发射后4 - 5天）及飞行后不同天数测量循环皮质醇（CS）、PRL、GH和IGF-1水平。
CS浓度未发现显著变化。飞行中PRL降低而GH和IGF-1升高（p < 0.05）。飞行后与飞行前相比未发现统计学上相关的激素变化。
观察到的激素变化与最初的假设一致，即太空飞行可能激活中枢神经系统肾上腺素能通路。这些变化发生在没有两种典型应激标志物（即CS和PRL升高）的情况下，从而排除了急性应激对结果的任何非特异性影响。与在实验动物和人类中进行的真实和模拟微重力研究的最新结果一致，这些数据支持了在太空飞行期间人类中枢神经系统肾上腺素能通路也被激活的假设。
