title: Uncoupler- and hypoxia-induced damage in the working rat heart and its treatment. II. Hypoxic reduction of aortic flow and its reversal.
abstract: In the working rat heart we investigated heart function (aortic and coronary flow) during a normoxic, a hypoxic, and a reoxygenation phase after hypoxia. A depressed heart function was obtained by limiting oxygen supply and reducing left ventricular filling pressure (preload). After hypoxic perfusion for about 90 min, reoxygenation resulted in a 50% decrease of aortic flow. Lactate production and release increased immediately after oxygen deprivation and reached a maximum after about 35 min of hypoxia. Following reoxygenation, lactate release decreased. Lactate dehydrogenase became significant after reoxygenation. After stabilization of aortic flow at 50% in the reoxygenation phase different reagents were examined for their influence on heart performance. 1.5 mM of 2-Mercaptopropionylglycine (MPG) significantly increased aortic flow by 40%. The oxidized form of MPG (ox-MPG) at a concentration of 0.6 mM increased aortic flow by 125%. A molecular mechanism is proposed involving reorientation of the ATPase molecules at their membrane sites.
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography; D004734:Energy Metabolism / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008929:Mitochondria, Heart / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000201:enzymology; D051381:Rats; D013438:Sulfhydryl Compounds / Q000494:pharmacology*; D008625:Tiopronin / Q000494:pharmacology
chemical_list: D007773:Lactates; D013438:Sulfhydryl Compounds; D019344:Lactic Acid; D008625:Tiopronin; D007770:L-Lactate Dehydrogenase