[Microcirculation of skeletal muscle after ischemia and reperfusion]

The postischemic reperfusion-damage in the microcirculation of skeletal muscle is characterized by 1) heterogenous capillary perfusion with capillary perfusion deficiency ("no reflow"), 2) microvascular accumulation of leukocytes, which adhere to the endothelium of postcapillary venules, and 3) increase of vessel permeability with swelling of endothelial cells and with interstitial edema. Two models of pathomechanism may be differentiated: The capillary perfusion-deficiency of the no-reflow phenomenon prolongs the duration of ischemia extending the period of postischemic reperfusion and induces the tissue-damage by further decrease of tissue-pH, by loss of energy rich phosphates and by a deficit of oxygen supply to tissue. On the other hand, reperfusion with consecutive reentry of molecular oxygen into the microvasculature provokes the formation of oxygen-radicals and the accumulation of leukocytes adhering to the endothelium of postcapillary venules ("reflow-paradox"). The activated white blood cells release additional oxygen-radicals and deliver aggressive mediators, such as proteases, cytokines and eicosanoids, which have chemotactic influence on leukocytes. This results in a vicious circle in which oxygen-radicals and mediators are responsible for the augmentation of postischemic tissue-damage. Prophylactic isovolemic hemodilution to a hematocrit of 30% with dextran 60 reduces the postischemic capillary perfusion deficiency (no reflow); therapy with "oxygen radical scavengers" and xanthinoxydase-inhibitors reduces accumulation/adherence of leukocytes as well as the damage to the endothelial lining with increased microvascular permeability (reflow-paradox). Intermittent reperfusion/reoxygenation influences both components of postischemic microcirculation damage and is therefore a simple clinical approach for reducing the ischemia/reperfusion-syndrome in elective surgery.