The sink action of cerebrospinal fluid in uremia.
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.
D000136:Acid-Base Equilibrium; D000818:Animals; D001812:Blood-Brain Barrier; D001834:Body Water / Q000378:metabolism; D002540:Cerebral Cortex / Q000032:analysis; D002831:Choroid Plexus / Q000032:analysis; D007444:Inulin / Q000378:metabolism; D007457:Iodine Radioisotopes; D008297:Male; D009132:Muscles / Q000032:analysis; D009392:Nephrectomy; D011188:Potassium / Q000032:analysis / Q000134:cerebrospinal fluid; D051381:Rats; D012964:Sodium / Q000032:analysis / Q000134:cerebrospinal fluid; D014508:Urea / Q000378:metabolism; D014511:Uremia / Q000134:cerebrospinal fluid* / Q000378:metabolism
D007457:Iodine Radioisotopes; D014508:Urea; D007444:Inulin; D012964:Sodium; D011188:Potassium