Hise M A, Johanson C E
Eur Neurol. 1979;18(5):328-37. doi: 10.1159/000115097.
The distribution of water, electrolytes and non-electrolytes in various compartments of the central nervous system was analyzed in rats subjected to various stages of uremia. After bilateral nephrectomy for various periods of time ranging from 1 to 18 h, there is a progressive hyperkalemia, hyponatremia and metabolic acidosis. Although the cerebrospinal fluid (CSF) [K] progressively increases to a concentration of 6 mmol/l at 48 h post-nephrectomy, the ratio of CSF [K]/plasma [K] remains relatively constant throughout the duration of the uremic challenge; on the other hand, the concentration gradient for Na (CSF to plasma) markedly increases with progression of uremia. The steady rise in cellular [K] in both the choroid plexus and in at least one compartment of the cerebral cortex is presumably a reflection of stimulattion of the Na-K pump caused by a build-up in [K] in the extracellular fluids of the brain. The blood-brain and blood-CSF barrier systems to both 14C-urea and 131I remain intact 24--48 h after nephrectomy; and there is not any evidence of cerebral edema at any stage of uremia. Thus, several lines of evidence indicate that the CSF-sink effect is maintained even in advanced uremia.
对处于不同尿毒症阶段的大鼠中枢神经系统各腔室中的水、电解质和非电解质分布进行了分析。在双侧肾切除术后1至18小时的不同时间段内,出现了进行性高钾血症、低钠血症和代谢性酸中毒。尽管脑脊液(CSF)[K]在肾切除术后48小时逐渐升高至6 mmol/L的浓度,但在整个尿毒症激发过程中,脑脊液[K]/血浆[K]的比值保持相对恒定;另一方面,Na(脑脊液至血浆)的浓度梯度随着尿毒症的进展而显著增加。脉络丛和大脑皮层至少一个腔室中细胞内[K]的持续升高可能反映了脑细胞外液中[K]积累对Na-K泵的刺激。肾切除术后24至48小时,血脑屏障和血脑脊液屏障对14C-尿素和131I均保持完整;并且在尿毒症的任何阶段都没有脑水肿的证据。因此,多条证据表明,即使在晚期尿毒症中,脑脊液-汇效应仍得以维持。