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Titolo:
A global approach to energy metabolism in an experimental model of sepsis
Autore:
LHer, E; Sebert, P;
Indirizzi:
Univ Hosp, Med Intens Care Unit, Brest, France Univ Hosp Brest FranceUniv Hosp, Med Intens Care Unit, Brest, France Brest Med Univ, Dept Physiol, Brest, France Brest Med Univ Brest FranceBrest Med Univ, Dept Physiol, Brest, France
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
fascicolo: 8, volume: 164, anno: 2001,
pagine: 1444 - 1447
SICI:
1073-449X(20011015)164:8<1444:AGATEM>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULTIPLE ORGAN FAILURE; SEPTIC SHOCK; LACTIC-ACIDOSIS; SKELETAL-MUSCLE; LACTATE; TISSUE; FIBERS; FLUX; MITOCHONDRIA; HYPOXIA;
Keywords:
glycolysis; lactate; mitochondrial function; sepsis; skeletal muscle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: L'Her, E CHU Cavale Blanche, F-29609 Brest, France CHU Cavale Blanche Brest France F-29609 , F-29609 Brest, France
Citazione:
E. L'Her e P. Sebert, "A global approach to energy metabolism in an experimental model of sepsis", AM J R CRIT, 164(8), 2001, pp. 1444-1447

Abstract

Disturbances in energy metabolism during sepsis are not clearly understood. The aim of the study was to globally assess the energy drive in septic rat myocytes, studying both glycolysis rates and mitochondrial maximal activities together, using recent fn vitro techniques. Measurements were assessedbefore (H0) and. 4 h after sepsis induction (H4). Hyperlactatemia was observed in all septic animals ([lactate] = 1.2 +/- 0.3 mmol/L at H0 versus 3.3+/- 0.6 mmol/L at H4; p < 0.001). An enhanced glycolysis rate was observedin both aerobic (J(A) = 7.2 +/- 0.9 at H0 versus 18.2 +/- 4.1 nmol glucose/min/g at H4; p < 0.05) and anaerobic (J(B) = 7.5 +/- 1.2 at H0 versus 15.4+/- 3.4 p,mol glucose/min/g at H4; p < 0.05) fluxes, associated with a selective significant pyruvate-malate-dependent oxygen consumption rate decrease (Vo(2)-PM = 0.144 +/- 0.008 at H0 versus 0.113 +/- 0.007 mu mol O-2/h/mgat H4; p < 0.05). This oxygen consumption decrease can be interpreted either as a complex I and/or a complex I-ubiquinone relation alteration. Our results are consistent with the hypothesis that an altered mitochondrial function during sepsis is responsible, at least in part, for hyperlactatemia, which is thus a consequence of an increased glycolysis rate.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 10:12:30