Effect of NaHCO3 on cardiac energy metabolism and contractile function during hypoxemia

Objective: To examine the impact of administration of NaHCO3 on contractili ty and energy metabolism of the myocardium during hypoxemia. Methods: Regional myocardial hypoxia was induced in the left anterior desce nding (LAD) artery myocardium in anesthetized, open-chest dogs, using a per fusion circuit between the right atrium and the LAD artery, and a membrane oxygenator. The rate of flow in LAD artery was maintained constant with the use of a roller pump. During hypoxia, eight dogs were administered isotoni c NaHCO3 in the circuit and six other dogs received equimolar NaCl, Myocard ial contractile function was assessed using sonomicrometry for measurement of percentage of systolic shortening and preload recruitable stroke work. O xygen consumption and:the rate of appearance of lactate were measured, Clam p-frozen tissue samples were obtained at the end of the experiment from the hypoxic LAD myocardium and the nonhypoxic circumflex myocardium for measur ement of tissue lactate level. Results: During hypoxia, there was a significant decrease in oxygen consump tion by the LAD myocardium (35 +/- 7 mu mol/min in the NaCl group and 40 +/ - 7 mu mol/min in the NaHCO3 group during hypoxia vs. 131 +/- 11 mu mol/min during aerobic perfusion). There was also a significant decrease in myocar dial contractility as measured by percentage of systolic shortening (14 +/- 3% to -8 +/- 3%); NaHCO3 infusion during hypoxia did not improve myocardia l contractility (-7 +/- 2%), Similar results were obtained with measurement s of preload recruitable stroke work. The rate of production of lactate dur ing hypoxia was substantially lower than expected, based on the calculated oxygen deficit, and was not significantly increased by the administration o f NaHCO3 (33 +/- 9 mu mol/min in the NaCl group and 51 +/- 5 mu mol/min in the NaHCO3 group). Tissue lactate was not statistically different in the hy poxic myocardium supplied by the LAD artery and the nonhypoxic myocardium s upplied by the circumflex artery in either group. Conclusion: The response of the myocardium to hypoxia is to decrease its me chanical work and metabolic demand. The infusion of NaHCO3 did not enhance myocardial contractile function or flux in glycolysis during hypoxia, We sp eculate that this diminished mechanical work and metabolic demand may repre sent an adaptive response to preserve cellular integrity until oxygen deliv ery is restored.