Hanna Krauss, Jacek Kozlik, Paweł Chęciński, Przemysław Sosnowski, Kinga Mikrut, Łukasz Dzieciuchowicz
Med Sci Monit 1999; 5(3): BR410-414
Background: Tissue ischemia leads towards a significant depletion of cellular high-energy compounds. Kinins stabilize the pool of cellular high-energy compounds during ischemia and reperfusion. Their protective action mechanism remains partially understood. The purpose of this study was to determine the influence of kinins on the activity of selected Krebs cycle and pentose phosphate pathway enzymes as well as on levels of cellular high-energy compounds during ischemia and reperfusion.
Material/Methods: We used an experimental model of ischemia-reperfusion in the rats hind limb. Placebo, bradykinin, captopril or captopril with bradykinin receptor antagonists were administered intraperitoneally before reperfusion. We measured the levels of adenine nucleotides as well as isocitrate dehydrogenase (EC 184.108.40.206) and glucose-6-phosphate dehydrogenase activities (EC 220.127.116.11) in skeletal muscles during ischemia and the 1st, 3rd and 10th minute of reperfusion.
Results: Ischemia-reperfusion led to a significant reduction of adenyl nucleotide levels and enzymes activities. The administration of captopril and bradykinin produced a significant decrease of measured values. Bradykinin receptor antagonists suppressed the beneficial influence of captopril.
Conclusions: Kinins that activate Krebs cycle and pentose phosphate pathway enzymes exert a protective effect on the energetic balance in rat skeletal muscles, during ischemia and reperfusion.
Keywords: adenylate energy charde, Kinins, ischemia-reperfusion