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The host response to hypoxia in the critically ill 

The host response to hypoxia in the critically ill
The host response to hypoxia in the critically ill

Raghavan Raju

and Irshad H. Chaudry

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date: 16 May 2022

The hypoxic response of the host is complex. While the oxygen-sensing intracellular machinery attempts to restore cellular homeostasis by augmenting respiration and blood flow, events such as severe haemorrhage lead to whole body hypoxia and decreased mitochondrial function. Immunological perturbations following severe haemorrhage may result in multiple organ dysfunction and sepsis, while impaired perfusion may lead to microvascular injury and local hypoxia. Trauma-haemorrhage or hypoxic exposure in animals causes a systemic inflammatory response, decreased antigen presentation by peritoneal macrophages, hypoxaemia and initiation of endoplasmic reticulum stress. In response, the protein level of the oxygen-sensing transcription factor, hypoxia inducible factor (HIF)-1 increases; this leads to the regulation of expression of a number of genes resulting in decreased mitochondrial ATP production, but enhanced glycolytic processes, thus shifting the energy balance. In addition, sustained tissue hypoxia leads to increased free radical production and cellular apoptosis. Though the initial host response to hypoxia may be protective, sustained hypoxia becomes detrimental to the tissues and the organism as a whole.

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