Left Ventricular Contractile and Energetic Dysfunction After Recovery from Acidosis

Abstract

It has been generally recognized that left ventricular (LV) contractile dysfunction during acidosis is almost reversible after correction of acidosis in crystalloidperfused hearts. In contrast, we have found that LV contractile function is paradoxically depressed after rapid correction of acidosis in blood-perfused hearts. To determine the mechanism of this phenomenon, we measured LV contractility (Emax), total mechanical energy (PVA), and myocardial oxygen consumption (Vo₂) before and after correction of hypercapnic acidosis in isolated cross-circulated dog hearts. During acidosis with CO₂ loading, Emax decreased significantly. During rapid correction of acidosis by CO₂ unloading, a transient overshoot of Emax and concomitant ventricular arrhythmias were followed by a paradoxical decrease in Emax and a significant increase in the oxygen cost of contractility. This result indicates that the postacidotic failing heart requires higher Vo₂ for a unit increase in Emax than the normal heart, which energetically resembles postischemic stunned myocardium. When dimethylamiloride, a selective Na₊-H₊ exchange inhibitor, was administered just before the correction of acidosis, the development of contractile and energetic abnormalities after correction of acidosis was almost completely prevented. Thus rapid correction of acidosis paradoxically depresses myocardial contractility and increases the oxygen cost of contractility through activation of the Na₊-H₊ exchange system. In addition, the blood-perfused heart behaves differently from the crystalloidperfused heart during the process of recovery from acidosis.