Increased oxygen cost of contractility in the endotoxemic porcine left ventricle

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Abstract
Objective—Myocardial oxygen consumption (MVO 2 ) in the septic myocardium is comparatively high in relation to the sepsis‐induced reduction in ventricular work. Our previous studies indicate that this energetic inefficiency is due to increased energy consumption in excitation–contraction (EC) coupling, i.e. myocardial calcium handling. Design—To further confirm this observation, we assessed the oxygen cost of contractility in anesthetized pigs before and 2 h after induction of endotoxemia (1 μg/kg endotoxin infusion over 1 h, Escherichia coli toxin, n=6). Baroreceptor reflexes were blocked by hexamethonium. Contractility was increased by stepwise dopamine infusions at baseline and 2 h after induction of endotoxemia. Oxygen cost of contractility was assessed as the relationship between myocardial contractility (E es or elastance) and non‐mechanical oxygen consumption (unloaded MVO 2 ), a measure of energy consumption in EC coupling or calcium handling. Results—Non‐mechanical oxygen consumption (unloaded MVO 2 ) was higher after endotoxin infusions than at baseline (0.641±0.05 vs 0.383±0.07 J/beat/100 g, p < 0.05). The relationship between unloaded MVO 2 and E es , constructed by the dopamine response, was highly linear both at baseline and endotoxemia (r 2 =0.76–0.99). However, endotoxin increased oxygen cost of contractility by ∼45% (baseline 0.06±0.03 vs endotoxin 0.09±0.04 J ml/mmHg/beat/100 g). Conclusion—Acute endotoxemia increases oxygen cost of contractility, a measure of energy consumed in EC coupling or myocardial calcium handling.