Effect of NaHCO3 on cardiac energy metabolism and contractile function during hypoxemia.
OBJECTIVE
To examine the impact of administration of NaHCO3 on contractility and energy metabolism of the myocardium during hypoxemia.


METHODS
Regional myocardial hypoxia was induced in the left anterior descending (LAD) artery myocardium in anesthetized, open-chest dogs, using a perfusion 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 isotonic NaHCO3 in the circuit and six other dogs received equimolar NaCl. Myocardial contractile function was assessed using sonomicrometry for measurement of percentage of systolic shortening and preload recruitable stroke work. Oxygen consumption and the rate of appearance of lactate were measured. Clamp-frozen tissue samples were obtained at the end of the experiment from the hypoxic LAD myocardium and the nonhypoxic circumflex myocardium for measurement of tissue lactate level.


RESULTS
During hypoxia, there was a significant decrease in oxygen consumption by the LAD myocardium (35 +/- 7 micromol/min in the NaCl group and 40 +/- 7 micromol/min in the NaHCO3 group during hypoxia vs. 131 +/- 11 micromol/min during aerobic perfusion). There was also a significant decrease in myocardial contractility as measured by percentage of systolic shortening (14 +/- 3% to -8 +/- 3%); NaHCO3 infusion during hypoxia did not improve myocardial contractility (-7 +/- 2%). Similar results were obtained with measurements of preload recruitable stroke work. The rate of production of lactate during hypoxia was substantially lower than expected, based on the calculated oxygen deficit, and was not significantly increased by the administration of NaHCO3 (33 +/- 9 micromol/min in the NaCl group and 51 +/- 5 micromol/min in the NaHCO3 group). Tissue lactate was not statistically different in the hypoxic myocardium supplied by the LAD artery and the nonhypoxic myocardium supplied by the circumflex artery in either group.


CONCLUSIONS
The response of the myocardium to hypoxia is to decrease its mechanical work and metabolic demand. The infusion of NaHCO3 did not enhance myocardial contractile function or flux in glycolysis during hypoxia. We speculate that this diminished mechanical work and metabolic demand may represent an adaptive response to preserve cellular integrity until oxygen delivery is restored.
University of Toronto and the Department of Medicine, St. Michael's Hospital, Toronto, Ontario, Canada.
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Kamel
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Mazer
D000140:Acidosis, Lactic / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D004195:Disease Models, Animal; D004285:Dogs; D004353:Drug Evaluation, Preclinical; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism* / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000150:complications* / Q000378:metabolism* / Q000503:physiopathology; D017682:Myocardial Stunning / Q000209:etiology; D010101:Oxygen Consumption / Q000187:drug effects; D017693:Sodium Bicarbonate / Q000494:pharmacology* / Q000627:therapeutic use*; D013318:Stroke Volume / Q000187:drug effects
D019344:Lactic Acid; D017693:Sodium Bicarbonate