Linked Life Data

2886767

Source:http://linkedlifedata.com/resource/pubmed/id/2886767

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8554
pubmed:dateCreated
1987-9-14
pubmed:abstractText
This hypothesis, presented to explain the cerebral oedema that sometimes occurs during treatment of diabetic ketoacidosis (DKA), is based on activation of the Na+/H+ exchanger, a ubiquitous plasma-membrane transport system that functions in the regulation of cytoplasmic pH. Experimental acidification of the cytoplasm with weak organic acids activates the exchanger and, in the presence of extracellular Na+, leads to cell swelling. This swelling is osmotic, secondary to a net gain in Na+ and the anion of the weak organic acid. In DKA, cytoplasmic acidification results from high levels of circulating weak organic acids (ketoacids and free fatty acids) and activation of Na+/H+ exchange would similarly be expected. Conditions during conventional treatment of DKA should favour even greater activation of the exchanger and additional cell swelling would be predicted. The hypothesis is consistent with the clinical observation that clinically apparent cerebral oedema occurs with improvement in the patient's acid-base status rather than at the peak of the ketoacidosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0140-6736
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
306-8
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Possible mechanism for cerebral oedema in diabetic ketoacidosis.
pubmed:publicationType
Journal Article