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Editorial
. 2011 Feb;114(2):239-42.
doi: 10.1097/ALN.0b013e3182070c66.

Targeting Hypoxia-induced Inflammation

Holger K Eltzschig
Editorial

Targeting Hypoxia-induced Inflammation

Holger K Eltzschig. Anesthesiology. 2011 Feb.
No abstract available

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Conflict of interest statement

Potential Conflict of Interest:H.K.E. has no conflict of interest.

Figures

Figure 1
Figure 1. Interdependent Relationship between Hypoxia and Inflammation
Exposure to ambient hypoxia triggers an acute inflammatory response in different organs, including the kidney, the intestine, the heart or the lungs. Hypoxia-induced inflammation can manifest itself as increased vascular leakage, accumulation of inflammatory cells in hypoxic organs, or release of inflammatory mediators, for example tumor necrosis factor (TNF)-α, IL6 or IL8. At the same time – and as shown here for acute lung injury - inflammation is associated with tissue hypoxia caused by dramatic increases in the demand for metabolites and oxygen by resident cells (e.g. pulmonary epithelia, vascular endothelia) and recruited inflammatory cells (e.g. neutrophils). At the same time, oxygen supply is attenuated due to pulmonary edema, airway plugging, or micro thrombi.
Figure 2
Figure 2. Proposed crosstalk pathways involved in multi-organ failure elicited by acute kidney injury (see Kim et al. Anesthesiology 2010)
See this image and copyright information in PMC

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