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 m embrane oxygenator in the coronary arterial perfusion circuit. Acidosi s [pH: 6.98 +/- 0.09 (SD), Pco(2): 91 +/- 25 mmHg in the coronary arte rial 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) lev el 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 oxyge n 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 acidos is than preacidosis. We conclude that acidosis results in LV contracti le dysfunction accompanied by an increased oxygen cost of contractilit y. This increased energy cost of the excitation-contraction coupling c an be accounted for by a decreased Ca2+ sensitivity of the contractile proteins during acidosis.