Journal of Applied Physiology, Vol 63, Issue 4 1591-1600, Copyright © 1987 by American Physiological Society
Chloride flux from blood to CSF: inhibition by furosemide and bumetanide
D. C. Johnson, S. Singer, B. Hoop and H. Kazemi
Pulmonary Unit, Massachusetts General Hospital, Boston.
Movement of chloride from blood to cerebrospinal fluid (CSF) is one of the
factors that may be involved in regulation of CSF [Cl-], which is important
to CSF acid-base balance. We made quantitative measurements of the
unidirectional flux of radiolabeled chloride between blood and CSF in
anesthetized dogs, using 38Cl, a short-lived isotope (half-life 37.3 min).
This allowed multiple studies to be performed in a given animal. A
three-compartment model for the blood, CSF, brain extracellular fluid, and
ventriculocisternal perfusion system was used to determine the flux rate.
With normocapnia, the flux was 0.01.1 min-1. The influx could be
reproducibly measured for three separate determinations in the same animal
over a period of 6 h, being 98 +/- 6% of the control first run on the
second run and 113 +/- 6% on the third. Furosemide and bumetanide,
inhibitors of sodium-coupled chloride movement, lowered the flux to 43 +/-
3% and 55 +/- 6% of control, respectively. The combination of hypercapnia
and furosemide lowered the influx to 63 +/- 9% of control. These results
indicate that a major mechanism of chloride entry into CSF is
sodium-coupled chloride transport.
