NADH content and lactate production in the perfused rabbit heart.
The influence of oxygen availability and absence of contractile activity on the NADH content and lactate production were investigated in the rabbit heart. Isolated hearts were perfused according to Langendorff with a modified Tyrode solution, saturated with a gas mixture containing either 95% O2:5% CO2 (control), 50% O2:5% CO2 in N2 (hypoxia), or 5% CO2 in N2 (anoxia). In another series of hearts cardiac arrest was induced by perfusion with Tyrode solution (95% O2:5% CO2) where the KCl concentration was increased to 15 mmol l-1 (hyperkalemia). Oxygen uptake (VO2) was similar in hypoxic and control hearts (P greater than 0.05), whereas lactate production was four-fold higher during hypoxia vs. control (P less than 0.01). Hyperkalemia resulted in a 60% decrease in VO2 (P less than 0.05), and no significant change in lactate production vs. control (P greater than 0.05). Both PCr and ATP were substantially decreased only during anoxia. Muscle NADH, whose changes reflect those within the mitochondria, averaged (+/- SE) 0.074 +/- 0.010, 0.153 +/- 0.016, 0.486 +/- 0.162 and 1.771 +/- 0.091 mmol kg-1 dry wt during control, hyperkalemia, hypoxia and anoxia, respectively. It is concluded that: muscle contraction during conditions of adequate oxygen supply results in an oxidation of mitochondrial NADH (presumably due to ADP stimulation of respiration), and a decreased oxygen availability results in an increase in NADH and an accelerated lactate production, although the VO2 is not affected.
D000818:Animals; D003326:Coronary Circulation; D005260:Female; D006321:Heart / Q000502:physiology*; D007773:Lactates / Q000096:biosynthesis*; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009243:NAD / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D010477:Perfusion; D010710:Phosphates / Q000378:metabolism; D011817:Rabbits
D007773:Lactates; D010710:Phosphates; D009243:NAD