Mitochondrial function in sepsis: respiratory versus leg muscle.
Patients with sepsis-induced multiple organ failure often experience muscle fatigue in both locomotive and respiratory muscles. Muscle fatigue extends intensive care unit stay, mostly in the form of prolonged weaning from the ventilator, and the recovery period after intensive care unit treatment due to general muscle fatigue. Muscle mitochondria are the main determinant of muscle fatigue and fatigability. Derangements in mitochondrial function in locomotive muscles have been described extensively both in animal models and patients with sepsis. Also, in respiratory muscle, mitochondrial function and content are impaired during sepsis. However, in septic patients with multiple organ failure, in locomotive muscle, lower levels of energy-rich compounds accompany the decreased mitochondrial content, whereas in respiratory muscle, the decreased mitochondrial content has no effect on cellular energy metabolism.
Fredriksson
Katarina
K
Department of Anesthesiology and Intensive Care, Clintec, Karolinska Institutet and University Hospital, Stockholm, Sweden.
Rooyackers
Olav
O
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D007866:Leg / Q000503:physiopathology; D008124:Locomotion; D008928:Mitochondria / Q000378:metabolism*; D009102:Multiple Organ Failure / Q000378:metabolism* / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000378:metabolism*; D009130:Muscle, Smooth / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D012137:Respiratory System / Q000378:metabolism* / Q000503:physiopathology; D018805:Sepsis / Q000378:metabolism* / Q000503:physiopathology
D010725:Phosphocreatine; D019344:Lactic Acid; D000255:Adenosine Triphosphate