What question did this study set out to answer?

To describe cytopathic hypoxia as an acquired cellular respiratory defect in sepsis and evaluate its underlying biochemical mechanisms and therapeutic relevance.

January 1, 2002Critical CareOpen Access

Bench-to-bedside review: Cytopathic hypoxia.

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Authors

MFMitchell P. FinkLinköping University

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Implication

Translational review uncovers intrinsic cellular respiration defects in sepsis models, highlighting the need for mitochondrial-targeted therapies.

Key Points

To describe cytopathic hypoxia as an acquired cellular respiratory defect in sepsis and evaluate its underlying biochemical mechanisms and therapeutic relevance.
Reviewed in vivo rodent models challenged with lipopolysaccharide and in vitro human enterocyte-like Caco-2 cells treated with a cytokine cocktail (TNF, IL-1beta, IFN-gamma).
Assessed proposed mechanisms of mitochondrial impairment, including nitric oxide inhibition of cytochrome a,a3, peroxynitrite toxicity, and poly(ADP-ribose) polymerase-1 (PARP-1) pathway activation.
Tissue oxygen consumption is diminished in endotoxemic rodents and cytokine-treated enterocytes independently of oxygen delivery or microvascular perfusion.
Activation of PARP-1 drives severe intracellular NAD+/NADH depletion, emerging as a central driver of impaired mitochondrial energy production in established sepsis.

Cite This Study

Mitchell P. Fink (2002) studied this question.

synapsesocial.com/papers/6a7429cf4b324a85266e8707 https://doi.org/10.1186/cc1824

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Implication

Translational review uncovers intrinsic cellular respiration defects in sepsis models, highlighting the need for mitochondrial-targeted therapies.

Bench-to-bedside review: Cytopathic hypoxia.

Discussion

Member takes

Implication

Key Points

Cite This Study

Bench-to-bedside review: Cytopathic hypoxia.

Discussion

Member takes

Implication

Key Points

Cite This Study

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