Abstract:
:The pathogenesis of sepsis-induced multiple organ failure may crucially depend on the development of mitochondrial dysfunction and consequent cellular energetic failure. According to this hypothesis, interventions aimed at preventing or reversing mitochondrial damage may have major clinical relevance, although the timing of such interventions will be critical to both ensuring benefit and avoiding harm. Early correction of tissue hypoxia, strict control of glycaemia, and modulation of oxidative and nitrosative stress may afford protection during the initial, acute systemic inflammatory response. The regulated induction of a hypometabolic state resembling hibernation may protect the cells from dying once energy failure has developed, allowing the possibility of functional recovery. Repair of damaged organelles through stimulation of mitochondrial biogenesis and reactivation of cellular metabolism may accelerate resolution of the multiple organ failure syndrome.
journal_name
Crit Carejournal_title
Critical care (London, England)authors
Protti A,Singer Mdoi
10.1186/cc5014subject
Has Abstractpub_date
2006-01-01 00:00:00pages
228issue
5eissn
1364-8535issn
1466-609Xpii
cc5014journal_volume
10pub_type
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