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失重状态下负水平衡的机制:一种假说。

Mechanism for negative water balance during weightlessness: an hypothesis.

作者信息

Greenleaf J E

出版信息

J Appl Physiol (1985). 1986 Jan;60(1):60-2. doi: 10.1152/jappl.1986.60.1.60.

DOI:10.1152/jappl.1986.60.1.60
PMID:3944046
Abstract

The mechanism for the apparent decrease in body fluid volume in astronauts during spaceflight remains obscure. The widespread postulate that the hypohydration is the result of the Henry-Gauer reflex, a diuresis caused by inhibition of vasopressin secretion resulting from increased left and perhaps right atrial (central) venous pressure, has not been established with direct measurements on astronauts. An hypothesis is proposed to account for fluid-electrolyte shifts during weightlessness. A moderate but transient increase in central venous pressure occurs when orbit is entered that is insufficient to activate the Henry-Gauer reflex but sufficient to stimulate the release of atrial natriuretic peptides. Increased sodium excretion would facilitate some increased urinary water loss. The resulting relatively dilute plasma and interstitial fluids would cause fluid to shift into the cellular space, resulting in edema in the head and trunk and inhibition of thirst and drinking. Thus the negative water balance in astronauts would be caused by a gradual natriuresis and diuresis coupled with reduced fluid intake.

摘要

太空飞行期间宇航员体液量明显减少的机制仍不清楚。普遍的假设认为,低水化是亨利 - 高尔反射的结果,即由于左心房(可能还有右心房)中心静脉压升高导致抗利尿激素分泌受抑制而引起的利尿,但这一假设尚未通过对宇航员的直接测量得到证实。本文提出了一个假说,以解释失重期间的液体 - 电解质转移。进入轨道时,中心静脉压会出现适度但短暂的升高,这种升高不足以激活亨利 - 高尔反射,但足以刺激心房利钠肽的释放。钠排泄增加会促进尿水流失的增加。由此产生的相对稀释的血浆和组织液会导致液体转移到细胞间隙,导致头和躯干水肿,并抑制口渴和饮水。因此,宇航员的负水平衡将由逐渐的利钠和利尿以及液体摄入量减少引起。

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