POSSIBLE MECHANISM FOR CEREBRAL OEDEMA IN DIABETIC KETOACIDOSIS
Identifieur interne : 004E45 ( Main/Exploration ); précédent : 004E44; suivant : 004E46POSSIBLE MECHANISM FOR CEREBRAL OEDEMA IN DIABETIC KETOACIDOSIS
Auteurs : Johna. Van Der Meulen [Canada, Royaume-Uni] ; Amira Klip [Canada, Royaume-Uni] ; Sergio Grinstein [Canada, Royaume-Uni]Source :
- The Lancet [ 0140-6736 ] ; 1987.
Abstract
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.
Url:
DOI: 10.1016/S0140-6736(87)90892-0
Affiliations:
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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.</div></front></TEI><affiliations><list><country><li>Canada</li><li>Royaume-Uni</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="Canada"><noRegion><name sortKey="Van Der Meulen, Johna" sort="Van Der Meulen, Johna" uniqKey="Van Der Meulen J" first="Johna." last="Van Der Meulen">Johna. Van Der Meulen</name></noRegion><name sortKey="Grinstein, Sergio" sort="Grinstein, Sergio" uniqKey="Grinstein S" first="Sergio" last="Grinstein">Sergio Grinstein</name><name sortKey="Klip, Amira" sort="Klip, Amira" uniqKey="Klip A" first="Amira" last="Klip">Amira Klip</name></country><country name="Royaume-Uni"><region name="Ontario"><name sortKey="Van Der Meulen, Johna" sort="Van Der Meulen, Johna" uniqKey="Van Der Meulen J" first="Johna." last="Van Der Meulen">Johna. Van Der Meulen</name></region><name sortKey="Grinstein, Sergio" sort="Grinstein, Sergio" uniqKey="Grinstein S" first="Sergio" last="Grinstein">Sergio Grinstein</name><name sortKey="Klip, Amira" sort="Klip, Amira" uniqKey="Klip A" first="Amira" last="Klip">Amira Klip</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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