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大鼠慢性肾衰竭伴贫血发展过程中对红细胞钠和钾的影响变化

Changing effects on erythrocyte sodium and potassium during the development of chronic renal failure with anaemia in rats.

作者信息

Thomas T H, Mason C, Illingworth K M

出版信息

Clin Sci (Lond). 1986 Dec;71(6):639-46. doi: 10.1042/cs0710639.

DOI:10.1042/cs0710639
PMID:3791865
Abstract

Rats were studied 7 days and 17 days after the onset of renal failure which was induced by a surgical technique. Plasma urea, creatinine (PCr) and potassium had increased after 7 days; plasma potassium increased much more after 17 days but PCr was slightly lower. Renal failure caused resetting of erythropoietic control to a lower level of packed cell volume (PCV). After 7 days renal failure some rats had a low PCV, whereas others still had a normal PCV apparently due to slower erythrocyte destruction of pre-renal failure cells. After 7 days renal failure, rats with a normal PCV had an increased erythrocyte membrane leak to potassium that resulted in a low erythrocyte potassium [K+]RBC. This was accompanied by an increase in active sodium pump units [increased ouabain sensitive sodium flux (Fo) and its rate constant (ko)] that caused erythrocyte sodium ([Na+]RBC) to fall. The increased active pump units retarded the fall in [K+]RBC and may have extended the life of the normal erythrocytes in the renal failure environment. The PCV was below normal in all rats after 17 days renal failure. [K+]RBC was increased and since ko was normal there appeared to be compensation to produce erythrocytes with reduced membrane leak to potassium with longer standing renal failure. PCr was only related to PCV after 17 days renal failure and not in the earlier phase of erythrocyte destruction. The changes in erythrocyte membrane permeability were very significantly related to PCV after 17 days.

摘要

采用外科技术诱导大鼠发生肾衰竭,分别在发病后7天和17天对其进行研究。肾衰竭7天后,血浆尿素、肌酐(PCr)和钾升高;17天后血浆钾升高更多,但PCr略低。肾衰竭导致红细胞生成控制重置,使红细胞压积(PCV)降至较低水平。肾衰竭7天后,一些大鼠的PCV较低,而另一些大鼠的PCV仍正常,这显然是由于肾衰竭前细胞的红细胞破坏较慢。肾衰竭7天后,PCV正常的大鼠红细胞膜对钾的渗漏增加,导致红细胞内钾离子([K+]RBC)水平降低。与此同时,活性钠泵单位增加(哇巴因敏感钠通量(Fo)及其速率常数(ko)增加),导致红细胞内钠([Na+]RBC)水平下降。活性泵单位增加减缓了[K+]RBC的下降,可能延长了正常红细胞在肾衰竭环境中的寿命。肾衰竭17天后,所有大鼠的PCV均低于正常水平。[K+]RBC升高,由于ko正常,在肾衰竭持续时间较长时,似乎出现了代偿,以产生膜对钾渗漏减少的红细胞。肾衰竭17天后,PCr仅与PCV相关,而在红细胞破坏的早期阶段则无此关联。17天后,红细胞膜通透性的变化与PCV密切相关。

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