Role of metabolic acidosis on cardiac mechanical performance during severe acute hypoxia and reoxygenation is small and transient.

OBJECTIVE

The aim was to determine whether the metabolic acidosis that develops during severe acute myocardial hypoxia improves or impairs the recovery of cardiac mechanical function during reoxygenation.

METHODS

Isolated rat hearts performed external work against a model of the rat systemic vascular impedance. Four groups of 10 hearts were used for mechanical studies. In these experiments, the hearts were subjected to normoxic ventilation for 15 min, hypoxic ventilation for 20 min, and reoxygenation for 60 min. The perfusate pH was either allowed to drift downward due to metabolic acidosis, or it was corrected to 7.4 as hypoxia or reoxygenation began. Mechanical performance was assessed by measuring heart rate and model "aortic" pressure and flow and by computing left ventricular mean, pulsatile, and total hydraulic power output and stroke work. A further four groups of 10 hearts were used for biochemical studies. In these experiments, myocardial high energy phosphates and calcium content were measured at the end of the period of hypoxia.

RESULTS

When no attempt was made to regulate the perfusate pH, it drifted downward from 7.40(SEM 0.01) to 7.33(0.01) during hypoxia and then to 7.25(0.02) during reoxygenation. All mechanical variables measured and computed were severely depressed by hypoxia, whether the pH was regulated or not. Left ventricular total hydraulic hydraulic power output decreased to less than 10% of the control value in all experiment groups and recovered to 86.7-91.2% of the control value after 60 min of reoxygenation. Mechanical recovery was most rapid when the correction of acidosis was delayed until reoxygenation was begun. After 5 min of reoxygenation, it had recovered to 65.5% of the control value compared with a 37.0% recovery when the pH was allowed to drift and 34.9% when the pH was corrected to 7.4 during hypoxia. However, the differences in power output became non-significant after 10 min of reoxygenation. Myocardial creatine phosphate and adenosine triphosphate concentrations were decreased by hypoxia whether the pH was corrected (63.0% and 26.9% relative to the control), or not (68.9% and 35.0% relative to the control) (not statistically significant), but total cell calcium was not affected.

CONCLUSIONS

In the isolated rat heart, correction of the moderate metabolic acidosis that developed during severe acute myocardial hypoxia improved the rate of mechanical recovery, but the effect was small and not sustained.