Reperfusion injury

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Reperfusion injury refers to damage to tissue caused when blood supply returns to the tissue after a period of ischemia. The absence of oxygen and nutrients from blood creates a condition in which the restoration of circulation results in inflammation and oxidative damage from the oxygen rather than restoration of normal function.

The damage of reperfusion injury is due in part to the inflammatory response of damaged tissues. White blood cells carried to the area by the newly returning blood release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage (Clark, 2005). The reintroduction of oxygen with restored blood flow forms within cells that damage cellular proteins, DNA, and the plasma membrane. Damage to the cell's membrane may in turn cause the release of more free radicals. Leukocytes may also build up in small capillaries, obstructing them and leading to more ischemia (Clark, 2005).

Reperfusion injury plays a part in the brain's ischemic cascade, which is involved in stroke and brain trauma. Repeated bouts of ischemia and reperfusion injury also are thought to be a factor leading to the formation and failure to heal of chronic wounds such as pressure sores and diabetic foot ulcers (Mustoe, 2004). Continuous pressure limits blood supply and causes ischemia, and the inflammation occurs during reperfusion. As this process is repeated, it eventually damages tissue enough to cause a wound (Mustoe, 2004).

In prolonged Ischemia (60min. or more), Hypoxanthine is formed as breakdown product of ATP metabolism. The enzyme Xanthine dehydrogenase is converted to Xanthine oxidase. During reperfusion, the availability of oxygen enables xanthine oxidase to catalyze the oxidation of Xanthine dehydrogenase. Oxidation of Xanthine dehydrogenase results in molecular oxygen being converted into superoxide radicals and hydroxyl radicals; radicals are highly reactive due to a lone electron in their outer shell. These radicals attack cell membrane lipids, proteins, glycosaminoglycans, causing further damage.

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References

  1. Clark WM. 2005. Reperfusion Injury in Stroke. Emedicine.com.
  2. Mustoe T. Understanding chronic wounds: a unifying hypothesis on their pathogenesis and implications for therapy. The American Journal of Surgery, Volume 187, Issue 5, Supplement 1, May 2004, Pages S65-S70.
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