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Lactate and shock state: the metabolic view
1Service de Réanimation Médicale, CHU Brabois, 54500 Vandoeuvre les Nancy, Nancy, France. b.levy@chu-nancy.fr
Current Opinion in Critical Care
|July 1, 2006
Summary
Severe sepsis and septic shock can cause elevated lactate levels, but not always due to hypoxia. Recent findings suggest enhanced aerobic glycolysis in skeletal muscles contributes to hyperlactataemia, challenging the traditional view.
Area of Science:
- Physiology
- Biochemistry
- Critical Care Medicine
Background:
- The traditional understanding of severe sepsis and septic shock links elevated lactate to cellular hypoxia and anaerobic glycolysis.
- Emerging research questions the sole reliance on hypoxia as the cause of lactate accumulation in sepsis.
Purpose of the Study:
- To discuss the hypothesis that lactate formation during sepsis is not solely due to hypoxia.
- To outline recent advances in understanding lactate metabolism in shock.
Main Methods:
- Review of experimental data on glycolysis and glycogenolysis during hemorrhagic shock and sepsis.
- Analysis of studies investigating Na+/K+-ATPase stimulation and its link to lactate production.
- Examination of human studies on hyperkinetic septic shock and skeletal muscle lactate sources.
Main Results:
- Experimental data show stimulation of aerobic glycolysis and glycogenolysis in skeletal muscles, even without oxygen deficiency.
- This enhanced glycolysis is linked to Na+/K+-ATPase stimulation, particularly under epinephrine.
- Human studies indicate skeletal muscle as a primary lactate producer via aerobic glycolysis in hyperkinetic septic shock.
Conclusions:
- Sepsis is characterized by a hypermetabolic state with increased glycolysis and hyperlactataemia.
- Elevated lactate levels in sepsis do not always indicate hypoxia.
- In hyperkinetic states, increased lactate production is often due to aerobic glycolysis, not hypoxia.