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Titolo:
Effects of cardiogenic shock on lactate and glucose metabolism after heartsurgery
Autore:
Chiolero, RL; Revelly, JP; Leverve, X; Gersbach, P; Cayeux, MC; Berger, MM; Tappy, L;
Indirizzi:
Ctr Hosp Univ Vaudois, Surg Intens Care Unit, Lausanne, Switzerland Ctr Hosp Univ Vaudois Lausanne Switzerland Unit, Lausanne, Switzerland Ctr Hosp Univ Vaudois, Dept Anesthesia, Lausanne, Switzerland Ctr Hosp Univ Vaudois Lausanne Switzerland hesia, Lausanne, Switzerland CHU Grenoble, Lab Bioenerget, F-38043 Grenoble, France CHU Grenoble Grenoble France F-38043 ioenerget, F-38043 Grenoble, France CHU Grenoble, Med Intens Care Unit, F-38043 Grenoble, France CHU GrenobleGrenoble France F-38043 Care Unit, F-38043 Grenoble, France Fac Med, Grenoble, France Fac Med Grenoble FranceFac Med, Grenoble, France CHU Vaudois, Dept Cardiovasc Surg, CH-1011 Lausanne, Switzerland CHU Vaudois Lausanne Switzerland CH-1011 , CH-1011 Lausanne, Switzerland Univ Lausanne, Inst Physiol, Lausanne, Switzerland Univ Lausanne Lausanne Switzerland Inst Physiol, Lausanne, Switzerland
Titolo Testata:
CRITICAL CARE MEDICINE
fascicolo: 12, volume: 28, anno: 2000,
pagine: 3784 - 3791
SICI:
0090-3493(200012)28:12<3784:EOCSOL>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONINVASIVE ASSESSMENT; ENERGY-EXPENDITURE; GLYCOGEN KINETICS; LACTIC-ACIDOSIS; SODIUM LACTATE; GLUCONEOGENESIS; HUMANS; OXIDATION; HYPOXIA; OXYGEN;
Keywords:
lactate metabolism; lactic acidosis; glucose metabolism; cardiogenic shock; cardiac surgery; critical care; glucose turnover;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Chiolero, RL Univ Hosp, Surg Intens Care Unit, Dept Anesthesia, CHUV-BH 10, CH-1011 Lausanne, Switzerland Univ Hosp CHUV-BH 10 Lausanne Switzerland CH-1011 witzerland
Citazione:
R.L. Chiolero et al., "Effects of cardiogenic shock on lactate and glucose metabolism after heartsurgery", CRIT CARE M, 28(12), 2000, pp. 3784-3791

Abstract

Background: Hyperlactatemia is a prominent feature of cardiogenic shock. It can be attributed to increased tissue production of lactate related to dysoxia and to impaired utilization of lactate caused by liver and tissue underperfusion, The aim of this prospective observational study was to determine the relative importance of these mechanisms during cardiogenic shock. Patients: Two groups of subjects were compared: seven cardiac surgery patients with postoperative cardiogenic shock and seven healthy volunteers. Methods: Lactate metabolism was assessed by using two independent methods:a) a pharmacokinetic approach based on lactate plasma level decay after the infusion of 2.5 mmol . kg(-1) of sodium lactate; and b) an isotope dilution technique for which the transformation of [C-13]lactate into [C-13]glucose and (CO2)-C-13 was measured. Glucose turnover was determined using 6,6(2)H(2)-glucose. Results: All patients suffered from profound shock requiring high doses ofinotropes and vasopressors. Mean arterial lactate amounted to 7.8 +/- 3.4 mmol . L-1 and mean pH to 7.25 +/- 0.07, Lactate clearance was not different in the patients and controls (7.8 +/- 3.4 vs. 10.3 +/- 2.1 mL . kg(-1) . min(-1)). By contrast, lactate production was markedly enhanced in the patients (33.6 +/- 16.4 vs. 9.6 +/- 2.2 mu mol . kg(-1) . min(-1); p < .01), Exogenous [C-13]lactate oxidation was not different (107 +/- 37 vs. 103 +/- 4mmol), and transformation of [C-13]lactate into [C-13]glucose was not different (20.0 +/- 13.7 vs, 15.2% +/- 6.0% of exogenous lactate), Endogenous glucose production was markedly increased in the patients (1.95 +/- 0.26 vs.5.3 +/- 3.0 mg . kg(-1) . min(-1); p < .05 [10.8 +/- 1.4 vs. 29.4 +/- 16.7mu mol . kg(-1) min(-1)]), whereas net carbohydrate oxidation was not different (1.7 +/- 0.5 vs, 1.3 +/- 0.3 mg . kg(-1) . min(-1) [9.4 +/- 2.8 vs. 7.2 +/- 1.7 mu mol . kg(-1) . min(-1)]). Conclusions Hyperlactatemia in early postoperative cardiogenic shock was mainly related to increased tissue lactate production, whereas alterations of lactate utilization played only a minor role. patients had hyperglycemia and increased nonoxidative glucose disposal, suggesting that glucose-induced stimulation of tissue glucose uptake and glycolysis may contribute significantly to hyperlactatemia.

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Documento generato il 19/01/20 alle ore 20:41:54