Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | American Journal of Physiology: Heart and Circulatory Physiology |
| Vol/bind | 284 |
| Udgave nummer | 3 |
| Sider (fra-til) | H1028-34 |
| ISSN | 0363-6135 |
| DOI | |
| Status | Udgivet - 2002 |
Bibliografisk note
Keywords: Adult; Aerobiosis; Arm; Arteries; Endotoxemia; Endotoxins; Epinephrine; Fever; Humans; Hypokalemia; Kidney; Lactic Acid; Leg; Lipopolysaccharides; Muscle, Skeletal; Potassium; Reference Values; Sodium-Potassium-Exchanging ATPase; Tumor Necrosis Factor-alpha; VeinsAdgang til dokumentet
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I: American Journal of Physiology: Heart and Circulatory Physiology, Bind 284, Nr. 3, 2002, s. H1028-34.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Endotoxemia stimulates skeletal muscle Na+-K+-ATPase and raises blood lactate under aerobic conditions in humans.
AU - Bundgaard, Henning
AU - Kjeldsen, Keld
AU - Suarez Krabbe, Karen
AU - van Hall, Gerrit
AU - Simonsen, Lene
AU - Qvist, Jesper
AU - Hansen, Christian Muff
AU - Moller, Kirsten
AU - Fonsmark, Lise
AU - Lav Madsen, Per
AU - Klarlund Pedersen, Bente
N1 - Keywords: Adult; Aerobiosis; Arm; Arteries; Endotoxemia; Endotoxins; Epinephrine; Fever; Humans; Hypokalemia; Kidney; Lactic Acid; Leg; Lipopolysaccharides; Muscle, Skeletal; Potassium; Reference Values; Sodium-Potassium-Exchanging ATPase; Tumor Necrosis Factor-alpha; Veins
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
U2 - 10.1152/ajpheart.00639.2002
DO - 10.1152/ajpheart.00639.2002
M3 - Journal article
C2 - 12446281
SN - 0363-6135
VL - 284
SP - H1028-34
JO - American Journal of Physiology: Heart and Circulatory Physiology
JF - American Journal of Physiology: Heart and Circulatory Physiology
IS - 3
ER -