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- W1568634900 abstract "The regulation of the CSF (Cl/sup -/) plays a key role in CNS acid-base homeostasis. The authors have shown in previous studies that chloride influx from blood to CSF is largely dependent upon sodium-coupled carrier mediated movement. Therefore, the mechanism of chloride outflux from CSF to brain was evaluated in anesthetized dogs using ventricular-cisternal perfusion (VCP) with the short-lived isotope /sup 38/Cl/sup -/ and dextran. The outflux of /sup 38/Cl/sup -/ from CSF was determined from the different movements between /sup 38/Cl/sup -/ and dextran using a one compartment model. VCP was performed at a rate of 1.4 ml/min for 14 min, and then slowed to 0.28 ml/min. The /sup 38/Cl/sup -/ activity decreased to a steady state level about 12% lower than that of dextran within 40-50 minutes. Under control conditions (19 runs in 7 dogs), the rate of chloride outflux was 0.059 +/- 0.004 min/sup -1/ (mean +/- SE). It was not significantly changed after the inclusion of bumetanide (10/sup -5/ molar) in the VCP fluid (n=6), which inhibits sodium-coupled Cl/sup -/ transport, or with acetazolamide 4.5 x 10/sup -3/ molar (n=4) which inhibits carbonic anhydrase. The authors conclude that chloride outflux from CSF is not dependent uponmore » sodium-coupled carrier mediated movement, which is in contrast with chloride influx from blood to CSF, nor is it dependent upon carbonic anhydrase activity.« less" @default.
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- W1568634900 date "1986-03-05" @default.
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- W1568634900 title "Effects of inhibitors on chloride outflux from CSF" @default.
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