Linked Life Data

2000998

Source:http://linkedlifedata.com/resource/pubmed/id/2000998

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 2
pubmed:dateCreated
1991-4-11
pubmed:abstractText
To investigate the role of protein kinase C (PKC) activation in the pathogenesis of endotoxin (ETX) shock, the in vivo effects of phorbol 12-myristate 13-acetate (PMA) on ETX-induced lethality and glucose dyshomeostasis were determined. Fed rats (300-400 g) were treated intravenously with incremental doses of Salmonella enteritidis ETX and either the vehicle, 110 mg/kg ip dimethyl sulfoxide (DMSO), or 0.5 mg/kg ip PMA dissolved in DMSO. PMA significantly increased ETX-induced lethality to doses of 1.0-20 mg/kg. PMA augmented the initial hyperglycemia, late hypoglycemia, and hyperlactacidemia after 1 mg/kg iv ETX to rats anesthetized with pentobarbital sodium. In contrast, 4 alpha-phorbol, a phorbol derivative that does not activate PKC, had no effect on either lethality or the glucose and lactate responses. Hyperinsulinemia after 1 mg/kg iv ETX was prolonged by PMA but not by 4 alpha-phorbol. Insulin tolerance testing (0.5 U/kg iv) produced an exaggerated hypoglycemic response in PMA-treated endotoxic (0.33 mg/kg) rats. Glucose tolerance to 1.2 g/kg iv was increased by ETX and PMA attenuated the increased tolerance. Thus PKC activation may be involved in the pathogenesis of lethal endotoxicosis and associated glucose dyshomeostasis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
260
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R494-502
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Augmentation of endotoxic lethality and glucose dyshomeostasis by phorbol ester.
pubmed:affiliation
Department of Physiology, Loyola University Chicago Medical Center, Maywood, Illinois 60153.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.