摘要: The effect of sepsis on tissue oxygenation is complex and often confusing. This in part due to the paucity data from patients (excluding whole-body studies), huge variation laboratory models which have utilised different species, organs cell lines, insults, study durations methods, fluid resuscitation regimens, end-points. An organ-variable redistribution microvascular flow undoubtedly occurs though its significance causing hypoxia remains questionable. A lower oxygen consumption recognised with an increasing severity sepsis, a better prognosis being seen those spontaneously achieving higher values global delivery consumption. However, septic (well-resuscitated) animal demonstrate increase tension. suggest adequate but impaired utilisation oxygen. As over 90% consumed by body for mitochondrial generation ATP oxidative phosphorylation, cellular defect strongly implicated. Mitochondrial dysfunction has been inconsistently demonstrated; closer inspection, short-term and/or ‘milder’ insult show no change or activity whereas longer duration more severe depressed function. borne out preliminary human studies. Reactive nitrogen species appear instrumental this dysfunction; they may also act as signalling mediators ‘shutdown’, possibly protective mechanism reduce turnover face decrease production.