Linked Life Data

1872805

Source:http://linkedlifedata.com/resource/pubmed/id/1872805

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1991-9-17
pubmed:abstractText
Recent studies showed that hyperammonaemia caused many of the metabolic changes in portacaval-shunted rats, a model of hepatic encephalopathy. These changes included a depression in the cerebral metabolic rate of glucose (CMRGlc), an indication of decreased brain function. 2. The purpose of the present experiments was to determine whether the depression of CMRGlc caused by ammonia is confined to certain brain structures, or whether the depression is an overall decrease in all structures, such as occurs in portacaval-shunted rats. To accomplish this objective, rats were made hyperammonaemic by giving them intraperitoneal injections of 40 units of urease/kg body wt. every 12 h; control rats received 0.154 m-NaCl. CMRGlc was measured 48 h after the first injection, by using quantitative autoradiography with [6-14C]glucose as a tracer. 3. The experimental rats had high plasma ammonia concentrations (control 70 nmol/ml, experimental 610 nmol/ml) and brain glutamine levels (control 5.4 mumol/ml). Hyperammonaemia decreased CMRGlc throughout the brain by an average of 19%. CMRGlc showed an inverse correlation with plasma ammonia, but a stronger correlation with the brain glutamine content. 4. Hyperammonaemia led to a decrease in CMRGlc throughout the brain that was indistinguishable from the pattern seen in portacaval-shunted rats. This is taken as further evidence that the cerebral depression found in portacaval-shunted rats is a consequence of hyperammonaemia. The observation that depression of CMRGlc correlated more closely with brain glutamine content than with plasma ammonia suggests that metabolism of ammonia is an important step in the pathological sequence.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-14033052, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-1702623, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-1872806, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-2018125, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-223799, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-2372051, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-2428933, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-2882529, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-3306479, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-3881042, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-4808789, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-5578559, http://linkedlifedata.com/resource/pubmed/commentcorrection/1872805-6834056
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0264-6021
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
277 ( Pt 3)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
693-6
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Hyperammonaemia depresses glucose consumption throughout the brain.
pubmed:affiliation
Department of Physiology and Biophysics, Chicago Medical School, North Chicago, IL 60064.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.