Bumetanide and cerebrospinal fluid acid-base variables during acute CO2 elevation.

The purpose of this study was to investigate the effects of bumetanide, an inhibitor of NaCl cotransport on cisternal cerebral spinal fluid (CSF) acid-base balance during acute respiratory acidosis (ARA). We measured blood and CSF acid-base variables in two groups (N = 7 in each) of anesthetized paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles (to eliminate saluresis). After baseline samples were obtained (-1 h) bumetanide (0.5 mg/kg) was administered intravenously within 15 min (group 2); group 1 received equal volume of diluted saline. ARA was induced 1 h later (0 h) and was maintained for 5 h. In both groups PaCO2 was maintained between 55 to 60 mm Hg. Mean cisternal CSF PCO2 was 42.8 +/- 2.6, and 43.8 +/- 2.5 mm Hg, respectively in group 1 and group 2 and rose approximately 20 mm Hg during ARA. In group 1, CSF [HCO3-] was 22.0 +/- 1.0, 24.8 +/- 0.6, and 25.4 +/- 1.6 mEq/L, respectively at 0, 2 1/2, and 5 h; respective values for group 2 were 22.9 +/- 1.5, 24.7 +/- 1.4, and 26.1 +/- 1.3 mEq/L. Comparing the two groups, respective values were not significantly different from each other. Similarly, between the two groups changes in CSF [Na(+)-Cl-] during ARA were not significantly different from each other. Based on our results we conclude that at the dose used in the present study bumetanide does not change ionic composition and acid-base balance of cisternal CSF when compared to controls. Because changes in CSF [Na(+)-Cl-] during ARA were similar in both groups, any inhibition of Cl- influx into CSF by bumetanide should have been proportional to that of Na+.