Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1988-2-12
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1591-600
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Chloride flux from blood to CSF: inhibition by furosemide and bumetanide.
pubmed:affiliation
Pulmonary Unit, Massachusetts General Hospital, Boston.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.