[Systemic effect of extremity-ischemia reperfusion surgical trauma. Assessment of tourniquet ischemia induced activation of poplymorphonuclear neutrophic granulocytes].

: Ischemia-reperfusion-injury represents a fundamental common pathway of tissue damage in a wide variety of disease processes, i.e. myocardial infarction, septic or hemorrhagic shock, multiple organ failure, trauma and organ transplantation. Ischemia-reperfusion-injury is said to be initiated by leukocyte accumulation and adhesion to vascular endothelium as well as oxygen free radicals playing a pivotal role in the pathogenesis of ischemia-reperfusion-injury. However, only few data exist for measuring influence of tourniquet-ischemia on the activation of granulocytes in humans. To assess the potential changes in activation of white blood cells immunophaenotyping (FacsScan, BD) of PMN was used in BTB-operated humans before and after 0, 5, 15, 30 and 120 min of tourniquet-ischemia of the lower and upper limb (no operation). We could show that tourniquet-ischemia (n = 20, 60-170 min) with operation significantly increased the CD 11b-expression to 149.5 +/- 73.4% (15 min after release of tourniquet, systemic, vs. bl: p < 0.05) and 160.1 +/- 55.1% (local, vs. bl: p < 0.001) and the CD 18-expression to 16.8 +/- 110.1% (systemic vs. bl: p < 0.01) and to 155.8 +/- 55.1% (local, vs. bl: p < 0.05). The tourniquet-ischemia of the upper limb without any operation (n = 10) induced an increase of the CD 11b-expression too (systemic, 149 +/- 76% and local 131 +/- 90%, both: p < 0.05 vs. bl). Furthermore there was a spontaneous release of free radical oxygen to 129.2 +/- 26.2% (systemic) und 154.8 +/- 35.9% (local: p < 0.01 vs. bl:) After stimulation by Phorbol-Myristat-Acetat (PMA) we demonstrated a decrease to 67.6 +/- 23.2% (systemic, p < 0.01 vs. bl) and to 68.3 +/- 15.6% (local, p < 0.01 vs. bl). These results indicate that ischemia-reperfusion-injury in humans induces a early measurable local and systemic activation of circulating PMN-granulocytes.