Table 1.

Proposed theories for the pathophysiology of reperfusion injury

PROPOSED THEORYDESCRIPTION
Oxidative stress3,5,6During ischemia, there is increased production of free radicals by local tissues and damaged mitochondria. On reperfusion, free radicals accumulate and destroy tissue because cellular antioxidants have been depleted
Intracellular calcium overload3,5ATP is depleted during ischemia. Consequently, function of membrane sodium-potassium ATPase pumps is compromised, leading to electrolyte disturbances and cell swelling. Intracellular hypercalcemia triggers pro-apoptotic signaling pathways that are further exacerbated when ATP supply is restored during reperfusion
Inflammation3,7Macrophages and damaged tissue secrete cytokines that promote neutrophilic recruitment. During reperfusion, this leads to accelerated neutrophilic extravasation of healthy tissue
Complement activation therapy35When ischemic tissue is reperfused, immunoglobulin M antibodies that were deposited onto ischemic tissues bind to complement proteins, upregulating local inflammation. Organ dysfunction and systemic inflammatory response syndrome have been reported in cases of major surgery or traumatic injury4
  • ATP—adenosine triphosphate, ATPase—adenosine triphosphatase.