Response to exercise and mechanical efficiency in non‐ischaemic stunning, induced by short‐term rapid pacing in dogs: a role for calcium?

Aim Rapid pacing ( RP ) is a regularly used model to induce heart failure in dogs. The aim of the study was to evaluate Ca 2+ handling, left ventricular ( LV ) contractile response during Ca 2+ administration compared to exercise, as well as oxygen consumption and mechanical efficiency after 48 h of RP . Methods Fifty‐three mongrel dogs were instrumented to measure LV pressure, LV fractional shortening, regional wall thickening and coronary blood flow. Contractile reserve was measured with isoproterenol and intravenous ( IV ) Ca 2+ administration. To assess the function of the sarcoplasmic reticulum ( SR ), post‐extrasystolic potentiation ( PESP ) and SR Ca 2+ uptake were measured. A graded treadmill test was performed in baseline and after RP ( n = 14). In a separate group of animals ( n = 5), myocardial performance and oxygen consumption were measured using a wide range of loading conditions. Results Left ventricular contractility was significantly decreased upon cessation of pacing. The contractile response to isoproterenol was blunted compared to a preserved response to IV Ca 2+ . Post‐extrasystolic potentiation was slightly increased after RP . Maximal velocity ( V max ) of SR Ca 2+ uptake was unchanged. Contractile response during exercise is attenuated after RP . External work is reduced, whereas oxygen consumption is preserved, provoking a reduced mechanical efficiency. Conclusion Forty‐eight‐hours RP provokes a reversible LV dysfunction, while the SR function and response to exogenous Ca 2+ are preserved. This is compatible with an intracellular functional remodelling to counteract Ca 2+ overload provoked by RP . Left ventricular dysfunction is accompanied by a reduced contractile reserve, but an unchanged oxygen consumption, illustrating an alteration in oxygen utilization.