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Objective: We investigated whether an increased oxygen cost of contractility and/or a decreased myofibrillar efficiency contribute to oxygen wastage of stunned myocardium. Because Ca2+-sensitizers may increase myofibrillar Ca2+-sensitivity without increasing cross-bridge cycling, we also investigated whether EMD 60263 restores myofibrillar efficiency and/or the oxygen cost of contractility. Methods: Regional fiber stress and strain were calculated from mesomyocardially implanted ultrasound crystals and left ventricular pressure in anesthetized pigs (n=18). Regional myocardial oxygen consumption (MVO2) was measured before contractility (end-systolic elastance, Ees) and total myofibrillar work (stress–strain area, SSA) were determined from stress–strain relationships. Atrial pacing at three heart rates and two doses of dobutamine were used to vary SSA and Ees, respectively. After stunning (two times 10-min ischemia followed by 30-min reperfusion), measurements were repeated following infusion of saline (n=8) or EMD 60263 (1.5 mg·kg−1 i.v., n=10). Linear regression was performed using: MVO2=α·SSA+β·Ees+γ·HR−1 (α−1, myofibrillar efficiency; β, oxygen cost of contractility; and γ, basal metabolism/min). Results: Stunning decreased SSA by 57% and Ees by 64%, without affecting MVO2, while increasing α by 71% and β by 134%, without affecting γ. From the wasted oxygen, 72% was used for myofibrillar work and 18% for excitation–contraction coupling. EMD 60263 restored both α and β. Conclusions: Oxygen wastage in stunning is predominantly caused by a decreased myofibrillar efficiency and to a lesser extent by an increased oxygen cost of contractility. Considering that EMD 60263 reversed both causes of oxygen wastage, it is most likely that this drug increases myofibrillar Ca2+-sensitivity without increasing myofibrillar cross-bridge cycling. [ABSTRACT FROM PUBLISHER]

Objective: In order to determine whether the relatively high oxygen consumption of stunned myocardium is related to decreased mechanical efficiency, myocardial oxygen consumption (MVO2) and its major determinants were studied in 10 open chest anaesthetised pigs. Methods: According to the time varying elastance concept, MVO2 is determined by contractility (Emax) and total mechanical work (PLA), which is the sum of the external work (EW) and potential energy (PE). Mechanical efficiency (EW/MVO2) equals the product of EW/PLA (=efficiency of energy transfer or EET) and PLA/MVO2. Eimx is the slope of the end systolic pressure-segment length relationship, determined by gradually clamping the aorta. PLA is the area enclosed by the end systolic pressure-segment length relationship and the pressure-segment length trajectory. EW is the area of the pressure-segment length loop. Systemic haemodynamics, regional segment shortening, and MVO2 were determined at baseline, during stunning (two sequences of 10 min occlusion and 30 min of reperfusion), after a subsequent 50 beats·min−1 increase in heart rate by atrial pacing and additional infusion of 2 μg·kg−1·min−1 dobutamine. Results: Stunning decreased segment shortening from 18.2(SEM 1.9)% to 10.2(1.5)%, MVO2 from 4.16(0.27) × 102 to 2.84(0.25) × 12 μ·mol·bear−1g−1, and Emax from 47(9) to 23(3) mm Hg·mm−1 (all p < 0.05). PLA decreased by 13(4)%, as EW decreased by 42(6)%, and PE tended to increase. Although EET decreased from 0.58(0.04) to 0.40(0.03) (p < 0.05), there was no decrease in the mechanical efficiency, as an increase in PE caused an increase in PLA/MVo, which compensated for the decrease in EET. Dobutamine infusion increased Emax and EW per beat to 120(23)% and 67(8)% of baseline, respectively, while MVO2 [4.12(0.53) μmol·beat−1·g−1] and EET [0.57(0.04)] returned to baseline. Conclusions: In stunned myocardium, mechanical efficiency is not decreased despite a decrease in EET. The increase in EET after dobutamine may explain the lack of the excessive increase in MVO2.Cardiovascular Research 1993;27:740-747 [ABSTRACT FROM PUBLISHER]

Study objective — The aim as to compare the responses of intracoronary infusions of ATP, an endothelium dependent vasodilator, with adenosine following brief ischaemia (10 min) and reperfusion in a model of myocardial stunning.Design — In group 1 (n=6), coronary blood flow and endocardial (endo) and epicardial (epi) percent segment length shortening were measured in the distribution of the left anterior descending coronary artery before and during maximal intracoronary infusions of either adenosine or ATP (20 (μg·kg−1·min−1). Measurements were obtained before and after myocardial stunning both at control heart rate and during atrial pacing (150 beats·min−1). In group 2 (n=6), myocardial blood flows by microspheres and arterial-venous lactate and oxygen differences were determined following the same ischaemia-reperfusion protocol to characterise transmural changes in blood flow and metabolism in this model of stunning.Experimental material — The experiments were done on 12 anaesthetised swine, weight 25-39 kg.Measurements and main results — In group 1, baseline endo and epi segment length shortening were 16(SD 3)% and 14(6)% and following reperfusion were reduced to 10(4)% and 8(6)% respectively (p<0.05). Prior to stunning, minimal coronary resistances during adenosine and ATP were 0.81(0.40) and 0.76(0.25) mm Hg·min·ml−1 respectively and following reperfusion were 0.86(0.31) (NS) and 0.85(0.23) (NS) mm Hg·min·ml−1 respectively. Infusion of either vasodilator enchanced function by 30% following reperfusion whereas no such effect was observed prior to ischaemia. In group 2, no maldistribution of blood flow was observed following the same ischaemia-reperfusion protocol to account for this vasodilator enhancement in function. Percent lactate extraction values were 29(11)% and 25(14)% at preischaemic control and paced heart rates respectively, and following reperfusion were lowered to 0(12)% without pacing (p<0.05) and −1(34)% during pacing (p<0.05).Conclusions — Brief ischaemia and reperfusion in swine induces myocardial stunning without altering the vasodilator responses of either ATP, an endothelium dependent vasodilator, or adenosine. Recruitment in postischaemic segment length shortening was observed during infusions of both vasodilators at a time when maldistribution of flow was not observed. Possible mechanisms include either enhanced washout of lactate from the reperfused myocardium or greater utilisation of substrates during higher blood flows. [ABSTRACT FROM PUBLISHER]