Linked Life Data

12446281

Source:http://linkedlifedata.com/resource/pubmed/id/12446281

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-2-11
pubmed:abstractText
We assessed the hypothesis that the epinephrine surge present during sepsis accelerates aerobic glycolysis and lactate production by increasing activity of skeletal muscle Na(+)-K(+)-ATPase. Healthy volunteers received an intravenous bolus of endotoxin or placebo in a randomized order on two different days. Endotoxemia induced a response resembling sepsis. Endotoxemia increased plasma epinephrine to a maximum at t = 2 h of 0.7 +/- 0.1 vs. 0.3 +/- 0.1 nmol/l (P < 0.05, n = 6-7). Endotoxemia reduced plasma K(+) reaching a nadir at t = 5 h of 3.3 +/- 0.1 vs. 3.8 +/- 0.1 mmol/l (P < 0.01, n = 6-7), followed by an increase to placebo level at t = 7-8 h. During the declining plasma K(+), a relative accumulation of K(+) was seen reaching a maximum at t = 6 h of 8.7 +/- 3.8 mmol/leg (P < 0.05). Plasma lactate increased to a maximum at t = 1 h of 2.5 +/- 0.5 vs. 0.9 +/- 0.1 mmol/l (P < 0.05, n = 8) in association with increased release of lactate from the legs. These changes were not associated with hypoperfusion or hypoxia. During the first 24 h after endotoxin infusion, renal K(+) excretion was 27 +/- 7 mmol, i.e., 58% higher than after placebo. Combination of the well-known stimulatory effect of catecholamines on skeletal muscle Na(+)-K(+)-ATPase activity, with the present confirmation of an expected Na(+)-K(+)- ATPase-induced decline in plasma K(+), suggests that the increased lactate release was due to increased Na(+)-K(+)-ATPase activity, supporting our hypothesis. Thus increased lactate levels in acutely and severely ill patients should not be managed only from the point of view that it reflects hypoxia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1028-34
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12446281-Adult, pubmed-meshheading:12446281-Aerobiosis, pubmed-meshheading:12446281-Arm, pubmed-meshheading:12446281-Arteries, pubmed-meshheading:12446281-Endotoxemia, pubmed-meshheading:12446281-Endotoxins, pubmed-meshheading:12446281-Epinephrine, pubmed-meshheading:12446281-Fever, pubmed-meshheading:12446281-Humans, pubmed-meshheading:12446281-Hypokalemia, pubmed-meshheading:12446281-Kidney, pubmed-meshheading:12446281-Lactic Acid, pubmed-meshheading:12446281-Leg, pubmed-meshheading:12446281-Lipopolysaccharides, pubmed-meshheading:12446281-Muscle, Skeletal, pubmed-meshheading:12446281-Potassium, pubmed-meshheading:12446281-Reference Values, pubmed-meshheading:12446281-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:12446281-Tumor Necrosis Factor-alpha, pubmed-meshheading:12446281-Veins
pubmed:year
2003
pubmed:articleTitle
Endotoxemia stimulates skeletal muscle Na+-K+-ATPase and raises blood lactate under aerobic conditions in humans.
pubmed:affiliation
Department of Medicine, University of Copenhagen, 2100 Copenhagen, Denmark. HenningBungaard@dadlnet.dk
pubmed:publicationType
Journal Article, Clinical Trial, Controlled Clinical Trial, Research Support, Non-U.S. Gov't