Hypercapnic acidosis increases oxygen cost of contractility in the dog left ventricle
Hata, K.; Goto, Y.; Kawaguchi, O.; Takasago, T.; Saeki, A.; Nishioka, T.; Suga, H.
American Journal of Physiology 266(2 Pt 2): H730-H740
1994
ISSN/ISBN: 0002-9513 PMID: 8141374 Document Number: 430979
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-max) and the relationship between myocardial oxygen consumption ( ovrhdot VO-2) and pressure-volume area (PVA; a measure of the LV total mechanical energy). Acidosis was stably maintained without hypoxia by appropriately mixing CO-2 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 lt 0.01) and PVA by 47 +- 12% (P lt 0.01) at a fixed LV volume. When the preacidosis E-max level was restored by Ca-2+ infusion during acidosis, unloaded ovrhdot VO-2 (the ovrhdot VO-2 intercept of the ovrhdot VO-2-PVA relation) exceeded the control value by 19 +- 17% (P lt 0.05), indicating that acidosis required higher ovrhdot VO-2, for nonmechanical activities at a matched E-max. Moreover, the oxygen cost of enhanced contractility (the incremental ratio of unloaded ovrhdot VO-2 to E-max) was 1.53 +- 0.40 times higher (P lt 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 Ca-2+ sensitivity of the contractile proteins during acidosis.