In vivo measurement of interstitial TxB2-concentrations in skeletal muscle during ischemia and reperfusion.

Abstract

Acute arterial occlusion of an extremity frequently leads to prolonged periods of ischemia of skeletal muscle1, 2. Reestablishment of blood flow to previously ischemic skeletal muscle initiates various biochemical cascades which may lead to the development of a reperfusion syndrome1, 2. This syndrome is characterized by a paradoxical impairment of nutritive blood flow during reperfusion and may further aggravate local tissue damage. Thus, most of the damage to skeletal muscle occurs after oxygenation is restored rather than during ischemia2. A sudden release of metabolites from postischemic muscle tissue may have additional profound systemic consequences like acute renal failure or fatal multiple organ failure2. It was estimated that one third of deaths from peripheral embolism may result from the metabolic events of local ischemia and reperfusion.