Effects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma.

Proopiomelanocortin (POMC) is expressed in pituitary, central nervous system, and in a few peripheral tissues. This study addresses the hypothesis that metabolic stressors, such as acidosis, may induce the release of POMC derivatives into the cardiovascular system not only from the pituitary but also from other sites of POMC expression. In our study, we investigated the liberation of POMC derivatives from peripheral tissues under a state of acidosis achieved by tourniquet-induced ischemia, alteration of lactate concentration, and base excess. In eight patients undergoing knee arthroplasty under spinal anesthesia, catheters were inserted into the femoral vein proximally to thigh tourniquet location. Blood was drawn from these catheters 5 min before and 40 s, 5 min, and 10 min after tourniquet deflation to measure plasma concentrations of N-acetyl-beta-endorphin immunoreactive material (IRM), beta-endorphin IRM, authentic beta-endorphin, adrenocorticotropin, lactate, pH, and base excess. In five of eight patients, we found a significant increase of beta-endorphin IRM levels 40 s after tourniquet deflation compared with predeflation levels; 5 and 10 min after tourniquet deflation, the beta-endorphin IRM levels were below the detection limit. Thus beta-endorphin IRM was released from ischemic limb tissues into the cardiovascular system. Only a small part of the determined beta-endorphin IRM corresponded to authentic beta-endorphin. Forty seconds after tourniquet deflation, the beta-endorphin IRM concentration correlated with base excess (r < 0.71; P < 0.05); no significant correlations were found with pH or lactate levels. Thus it was shown here for the first time that ischemic stress may induce the release of beta-endorphin IRM from nonpituitary tissues.