Tissue hypoxia | Â | Â |
---|---|---|
Boekstegers et al.[43] | Muscle PO2 in septic patients | No evidence of muscle hypoxia |
Sair et al.[44] | ||
Levy et al.[45] | ||
VanderMeer et al.[46] | Intestinal and bladder mucosal PO2 in septic animals | No evidence of mucosal hypoxia |
Rosser et al.[47] | ||
Hotchkiss and Karl [48] | Cellular oxygenation by using hypoxic marker ([18?F] fluoromisonidazole) in septic animals | No cellular hypoxia in muscle, heart, lung and brain |
Regueira et al.[49] | Measurements of HIF-1? in septic patients/animals | No relation between HIF-1? and lactate levels |
Textoris et al.[50] | ||
Opdam and Bellomo [51] | Lactate production by the lung in septic shock patients | Substantial lactate release by the lung |
Mitochondrial dysfunction | Â | Â |
Hotchkiss and Karl [48] | Measurements of ATP and PCr in muscle samples of septic animals/patients | No decrease in any of the indicators of mitochondrial function |
Alamdari et al.[53] | ||
Brealey et al.[54] | ||
Pyruvate dehydrogenase | Â | Â |
Alamdari et al.[53] | Mitochondrial PDH activity in septic animals/patients | No association between PDH deficit/dysfunction and lactate increase |
Jahoor et al.[55] | ||
Stacpoole et al.[56] | ||
Dichloroacetate lowers lactate levels by stimulating the PDH complex | ||
DO2 – VO2 mismatch |  |  |
Critical DO2 in septic patients as they approached death | No association between hyperlactatemia and decreased DO2 or impaired O2ER | |
Mira et al.[59] | Relationship between DO2/SvO2 and SAHL | No relationship between DO2/SvO2 was found |
Astiz et al.[60] | ||
Marik and Sibbald [65] | Increases in DO2 did not decrease lactate concentration in SAHL |