Journalartikel
Autorenliste: Matejec, R; Schulz, A; Harbach, HW; Uhlich, H; Hempelmann, G; Teschemacher, HR
Jahr der Veröffentlichung: 2004
Seiten: 1040-1045
Zeitschrift: Journal of Applied Physiology
Bandnummer: 97
Heftnummer: 3
ISSN: 8750-7587
eISSN: 1522-1601
DOI Link: https://doi.org/10.1152/japplphysiol.01292.2003
Verlag: American Physiological Society
Abstract:
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.
Zitierstile
Harvard-Zitierstil: Matejec, R., Schulz, A., Harbach, H., Uhlich, H., Hempelmann, G. and Teschemacher, H. (2004) Effects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma, Journal of Applied Physiology, 97(3), pp. 1040-1045. https://doi.org/10.1152/japplphysiol.01292.2003
APA-Zitierstil: Matejec, R., Schulz, A., Harbach, H., Uhlich, H., Hempelmann, G., & Teschemacher, H. (2004). Effects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma. Journal of Applied Physiology. 97(3), 1040-1045. https://doi.org/10.1152/japplphysiol.01292.2003
Schlagwörter
ANAEROBIC EXERCISE; authentic beta-endorphin in plasma; base excess; BETA-ENDORPHIN LEVELS; corticotroph- or melanotrophtype proopiomelanocortin systems; functional significance of proopiomelanocortin fragments in plasma; HUMAN PITUITARY; INVOLVEMENT; reperfusion; TREADMILL EXERCISE