HYPERCAPNIC ACIDOSIS INCREASES OXYGEN COST OF CONTRACTILITY IN THE DOG LEFT-VENTRICLE

The effect of acidosis on left ventricular (LV) mechanoenergetics was assessed in seven excised, cross-circulated dog hearts with the use of the frameworks of the contractility index (E,,) and the relationship between myocardial oxygen consumption (VO2) and pressure-volume area (PVA; a measure of the LV total mechanical energy). Acidosis was stably maintained without hypoxia by appropriately mixing CO2 and air in a membrane oxygenator in the coronary arterial perfusion circuit. Acidosis [pH: 6.98 +/- 0.09 (SD), Pco(2): 91 +/- 25 mmHg in the coronary arterial blood] decreased E(max) by 45 +/- 12% (P < 0.01) and PVA by 47 +/- 12% (P < 0.01) at a fixed LV volume. When the preacidosis E(max) level was restored by Ca2+ infusion during acidosis, unloaded Vo(2) (the Vo(2) intercept of the Vo(2)-PVA relation) exceeded the control value by 19 +/- 17% (P < 0.05), indicating that acidosis required higher Vo(2), for nonmechanical activities at a matched E,,. Moreover, the oxygen cost of enhanced contractility (the incremental ratio of unloaded Vo(2) to E(max)) was 1.53 +/- 0.40 times higher (P < 0.01) during acidosis than preacidosis. We conclude that acidosis results in LV contractile dysfunction accompanied by an increased oxygen cost of contractility. This increased energy cost of the excitation-contraction coupling can be accounted for by a decreased Ca2+ sensitivity of the contractile proteins during acidosis.