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对钠代谢进行调控以维持渗透压和容量稳态。

The control of sodium metabolism to maintain osmo- and volumehomeostasis.

作者信息

Reinhardt H W, Kaczmarczyk G, Mohnhaupt R, Simgen B

出版信息

Klin Wochenschr. 1982 Oct 1;60(19):1240-4. doi: 10.1007/BF01716730.

Abstract

Chronically instrumented female beagles were maintained in standardized environmental and dietary conditions allowing careful examination of the mechanisms governing sodium homeostasis. The experimental increase in left atrial pressure (obtained by a reversible mitral stenosis) is accompanied by an increase in sodium excretion (atrial natriuresis, AN). AN served as an experimental manoeuvre from which the mechanisms governing sodium homeostasis could be elucidated. The results allow the following conclusions: (1) The 'signals' arising from distension of the left atrium (e.g. expansion of the extracellular fluid volume) appear not to be a necessary prerequisite for the maintenance of sodium homeostasis. (2) The control mechanisms seem to be very sensitive to changes in total body sodium (TBS). A small reduction in TBS abolishes sodium eliminating processes e.g. saline diuresis, osmotic diuresis, AN. (3) It is probable that a natriuretic factor exists for sodium elimination. In summary, total body sodium appears to be controlled by a series of 'redundant' mechanisms which guarantee an appropriate strategy for the comfort and ultimate survival of the organism. At the moment it is impossible to quantitate the contributions made by the various mechanisms in the control of sodium metabolism.

摘要

长期植入仪器的雌性比格犬饲养在标准化的环境和饮食条件下,以便仔细研究钠稳态调节机制。通过可逆性二尖瓣狭窄使左心房压力实验性升高,同时伴有钠排泄增加(心房利钠,AN)。AN作为一种实验手段,借此可阐明钠稳态调节机制。结果得出以下结论:(1)左心房扩张产生的“信号”(如细胞外液量增加)似乎并非维持钠稳态的必要前提条件。(2)控制机制似乎对总体钠(TBS)变化非常敏感。TBS的小幅降低会消除钠排泄过程,如盐水利尿、渗透性利尿、AN。(3)很可能存在一种排钠因子用于钠排泄。总之,总体钠似乎受一系列“冗余”机制控制,这些机制确保了机体舒适和最终生存的适当策略。目前尚无法量化各种机制在钠代谢控制中的作用。

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