ACUTE RESPIRATORY-ACIDOSIS - LARGE-DOSE FUROSEMIDE AND CEREBROSPINAL-FLUID IONS

NaCl cotransport carrier is known to be involved in transepithelial fl uid absorption and secretion in various tissues. Recent studies indica te that Na-K-2Cl cotransport carrier also exists in the choroid plexus cells and that inhibition of the carrier decreases cerebrospinal flui d (CSF) production. In this study, we used large-dose intravenous furo semide, an inhibitor of Na-K-2Cl carrier, to determine the effects on cisternal CSF ionic composition in acute respiratory acidosis. In pent obarbital-anesthetized mechanically ventilated dogs, renal pedicles we re ligated to prevent furosemide-induced diuresis. The experimental gr oup (group II, n = 7) received 400 mg/kg of furosemide intravenously, and group I (control group, n = 7) received the vehicle. In group II, serial serum and CSF furosemide concentrations were similar to 10(-3) and 10(-5) mol/l, respec tively. During 5 h of acute respiratory acido sis in both groups, the mean arterial Pco(2) increased similar to 25 T orr, with comparable changes in CSF Pco(2). In both groups, CSF [HCO3- ] and [H+] rose similar to 3 meq/l and 20 neq/l, respectively. Changes in CSF [Na+], [K+], [Cl-], and [Na+ - Cl-] were also similar and were not significantly different from each other when the two groups were compared. These data show that furosemide at the dose that inhibits Na Cl cotransport carrier does not significantly alter ionic composition of cisternal CSF.