Abstract

The aim was to evaluate the hypothesis that the oxygen demand of stimulated myocardium is downregulated and ischaemia avoided when oxygen supply is limited. Isoprenaline stimulation during reduced coronary perfusion pressure or moderate coronary hypoxaemia was studied in relation to myocardial oxygen demand, power, and oxygen utilisation efficiency (O2Effic) in 19 anaesthetised open chest dogs. The left anterior descending coronary artery was perfused with normoxic blood at 100 or 60 mm Hg or with moderately hypoxic blood [CaO2 = 9.8(SEM 0.2) ml.dl-1] at 100 mm Hg. Myocardial oxygen demand was estimated from oxygen consumption (MVO2), and power index was computed from heart rate, left ventricular pressure, and segment shortening. O2Effic was calculated from power index divided by MVO2. Lactate extraction and contractile function were used as indices of myocardial ischaemia. Isoprenaline under control conditions increased coronary blood flow, MVO2, and power index, but did not alter lactate extraction. Reducing coronary perfusion pressure to 60 mm Hg decreased oxygen delivery by 31.6(5.7)% (p < 0.05). MVO2 fell by 26.6(8.6)% (p < 0.05), but power index and lactate extraction were not reduced. At reduced coronary perfusion pressure, isoprenaline-induced elevation of MVO2 decreased from 26.0(1.5) to 15.7(2.6) ml.min-1 x 100 g-1 (p < 0.05), but the isoprenaline-induced rise in power index was not significantly lessened, nor was lactate extraction altered. O2Effic was increased by reduced coronary perfusion pressure and by isoprenaline during reduced coronary perfusion pressure. Hypoxaemia increased coronary blood flow but did not alter oxygen delivery, MVO2 or power index. Isoprenaline-induced elevation of MVO2 decreased from 25.2(1.7) to 19.1(0.5) ml.min-1 x 100 g-1 (p < 0.05), and power index decreased by 33(9.1)% (p < 0.05). O2Effic was not altered by hypoxaemia or by isoprenaline during hypoxaemia. Oxygen demand of isoprenaline stimulated myocardium is downregulated and ischaemia is avoided when oxygen is limited. Downregulation of oxygen demand is achieved by increasing oxygen utilisation efficiency in the presence of reduced coronary perfusion pressure and by decreasing power in the presence of hypoxaemia.

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