高压环境下的肾功能。

Y S Park, J R Claybaugh, K Shiraki, M Mohri
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引用次数: 15

摘要

在混合气体饱和潜水(3-49.5 ATA)期间,每日尿流量增加约500 ml/天,液体摄入量和肾小球滤过率没有变化。利尿伴随着尿渗透压的显著降低和尿素、K+、Na+、Ca2+和无机磷酸盐(Pi)等溶质排泄的增加。尿渗透压的下降主要是由于自由水重吸收的减少,这与抑制不自觉的水分流失和随之而来的抗利尿激素(ADH)系统的抑制有关。尿素排泄的增加可能与由于抗利尿激素抑制而导致的收集管尿素重吸收的减少有关。K+排泄的增加是由于醛固酮增加、尿流量增加和不可渗透阴离子(如Pi)的排泄促进了远端小管的K+分泌。醛固酮系统的激活部分归因于早期高压利尿引起的短暂性脱水。在醛固酮分泌增强的情况下,Na+排泄增加,表明近端小管中的Na+运输受到明显抑制(机制未知)。Pi排泄增加,血浆甲状旁腺激素(PTH)水平无变化,这可能是由于近端小管中Na(+)-Pi共转运受到抑制。Ca2+排泄的增加可能是继发于近端小管Na+运输的抑制。关于近端管状Na+运输的精确信息对于理解高压条件下受损溶质运输的机制是重要的。
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Renal function in hyperbaric environment.

During mixed gas saturation diving (to 3-49.5 ATA) daily urine flow increases by about 500 ml/day, with no changes in fluid intake and glomerular filtration rate. The diuresis is accompanied by a significant decrease in urine osmolality and increase in excretion of such solutes as urea, K+, Na+, Ca2+ and inorganic phosphate (Pi). The fall in urine osmolality is mainly due to a reduction of free water reabsorption which is associated with a suppression of insensible water loss and the attendant inhibition of antidiuretic hormone (ADH) system. The increase in urea excretion may be associated with a reduction of urea reabsorption at the collecting duct as a consequence of ADH suppression. The rise in K+ excretion is due to a facilitated K+ secretion at the distal tubule as a result of increased aldosterone, urine flow and excretion of impermeable anions such as Pi. The activation of aldosterone system is partly attributed to a transient dehydration induced by early hyperbaric diuresis. The increase in Na+ excretion in the face of enhanced aldosterone secretion indicates that the Na+ transport in the proximal tubule is markedly inhibited (by unknown mechanism). The Pi excretion increases with no changes in plasma level of parathyroid hormone (PTH), thus it may be due to an inhibition of Na(+)-Pi cotransport in the proximal tubule. The increase in Ca2+ excretion may be secondary to the inhibition of Na+ transport at the proximal tubule. Precise information on the proximal tubular Na+ transport is important to understand the mechanisms of impaired solute transport under hyperbaric conditions.

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