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休克时的可逆性肾浓缩功能缺陷

Reversible renal concentrating defect in shock.

作者信息

Whang R, Brandfonbrener M

出版信息

Lancet. 1975 Feb 15;1(7903):372-4. doi: 10.1016/s0140-6736(75)91282-9.

Abstract

The loss of renal concentrating power in haemorrhagic shock is reversible upon correction of the shock state. Shock resulting from acute hypovolaemia leads to the following sequence of events: (1) diminished renal blood-flow; (2) decreased superficial cortical nephron perfusion; (3) continued juxtamedullary nephron perfusion; (4) enhanced proximal reabsorption of Na, Cl, and H23; (5) decreased delivery of these ions to the ascending limb, which results in diminished hypertonicity of the medullary interstitium. This hypotonicity is worsened by the "washout" effect on the interstitial hypertonicity caused by continued perfusion of the juxtamedullary vasa recta which results in (6) diminished renal concentrating capacity due to elimination of medullary hypertonicity. Replenishing blood-loss and correcting the hypovolaemic state "regenerates" the hypertonic renal medullary interstitium by (a) diminishing proximal reabsorption and allowing presentation of greater quantities of Na and Cl to the ascending-limb "pump", (b) restoring superficial cortical nephron perfusion, thereby decreasing juxtamedullary perfusion and in this manner eliminating medullary "washout".

摘要

失血性休克时肾浓缩功能的丧失在休克状态纠正后是可逆的。急性血容量不足导致的休克会引发以下一系列事件:(1)肾血流量减少;(2)浅表皮质肾单位灌注减少;(3)近髓肾单位持续灌注;(4)近端对钠、氯和水的重吸收增强;(5)这些离子向升支的输送减少,导致髓质间质高渗性降低。近髓直小血管持续灌注对间质高渗性产生“冲洗”效应,使这种低渗性恶化,导致(6)由于髓质高渗性消失,肾浓缩能力降低。补充失血并纠正血容量不足状态可通过以下方式“再生”高渗性肾髓质间质:(a)减少近端重吸收,使更多的钠和氯进入升支“泵”;(b)恢复浅表皮质肾单位灌注,从而减少近髓灌注,以此消除髓质“冲洗”。

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