Differential effects of various inotropic agents on the intracellular NADH redox level in the in vivo dog heart.

A similar inotropic response was elicited by either increasing heart rate or infusing noradrenaline or ouabain in the open-chest dog preparation. Changes in local coronary blood supply and intracellular NADH redox level produced by these inotropic interactions were examined. Contractile tension was measured using a strain gauge arch; coronary flow, using a thermistor probe; and NADH redox level, by surface fluorometry. For each inotropic agent, isometric tension increased by about 40%. However, the mean increase in coronary flow was 80 +/- 9.7% for adrenaline, 67 +/- 18% for tachycardia, and 1 +/- 10.8% for ouabain. The mean changes in intracellular NADH redox level were -17 +/- 4.4%, 49 +/- 8.4%, and -6 +/- 6.4% for noradrenaline, tachycardia, and ouabain, respectively. The time course of changes in the various parameters was different following the onset of each inotropic stimulus. Furthermore, inducing tachycardia while the heart was under the influence of the various inotropic agents caused a reduction in contractility at different rates. These results indicate a large variation in the oxygen cost of contraction produced by these inotropic interventions, and also demonstrate notable variations in the intracellular oxygen balance. The possible relation between the intracellular NADH level and the "mechanical reserve" of cardiac muscle is discussed.