Utilization of oxygen by the contractile apparatus is disturbed during reperfusion of post-ischaemic myocardium

• Published in: European heart journal 1995-11, Vol.16 (11), p.1476-1481
• Main Authors: SCHIPKE, J. D., SUNDERDIEK, U., KORBMACHER, B., SCHWANKE, U., ARNOLD, G.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Pressure; Blood Volume; blood-perfusion; cardiac efficiency; Cardiology. Vascular system; Coronary heart disease; Heart; isolated heart; Male; Medical sciences; MVO2; Myocardial Contraction; Myocardial Ischemia - physiopathology; Myocardial Reperfusion Injury - physiopathology; Myocardial stunning; Myocardium - metabolism; Oxygen Consumption; rabbit; Rabbits; ventricular function
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/oxfordjournals.eurheartj.a060767

Post-ischaemic ventricular function remains depressed ( = myocardial stunning) despite nearly normal coronary blood flow during reperfusion. In order to illuminate the causes of this phenomenon, we studied the relationship between ventricular function and myocardial oxygen consumption (MVO2tot) in experiments on 15 isolated rabbit hearts perfused with erythrocyte suspension (hct=30%). Left ventricular systolic function was assessed by measuring aortic flow (ml. min −1), peak systolic pressure (L VPmax), dPldtmax, and early relaxation in terms of dPldtmin during control and 30 min after the onset of reperfusion, following 20 min global no-flow ischaemia. The pressure-volume area was calculated as a measure of total mechanical energy. The external mechanical efficiency (Eext) was assessed from stroke work and MVO2torBoth contractile efficiency (Econ= inverse slope of the MVO2-PVA relationship) and MVO2 of the unloaded contracting heart (MVO2unl= basal MVO2 + MVO2 for excitation-contraction coupling) were calculated using pressure-volume area and MVO2tot Results: At matched heart rate (149 ± 30 vs 147 ± 31 min −1; mean ± SD) and end-diastolic volume (1.3 ± 0.2 ml), the systolic variables were significantly decreased in the stunned myocardium: aortic flow: 38 ± 13 vs9 ± 11 ml. min −1, LVPmax: 112 ±19 vs 74±18mmHg, and dP/dtmax: 1475 ±400 vs 1075 ±275 mmHg. s−1. Likewise, dP/dtmin was significantly impaired (− 1275 ±250 vs − 975 ±250). The decrease in pressure-volume area (570 ±280 vs 270±200mmHg. ml. 100g−1) was not statistically significant. In contrast, both Eext (0.75±0.29 vs 0.18±0.26 arbitrary units) and Econ (31 ± 18 vs 14± 7%) were significantly decreased, whereas MVO2tot (40±9 vs 34±8μl. beat−1. 100g−1) and MVO2unl (26±9 vs22±6μl. beat−1. 100g−1) were not. Summary: Ventricular function after brief episodes of ischaemia is decreased whereas MVO2tot is maintained, i.e. external efficiency is decreased. MVO2 for the unloaded contraction remained unchanged, indicating that MVO2for excitation-contraction coupling is inappropriately high for the depressed contractile state. The decreased contractile efficiency indicates further that O2 utilization of the contractile apparatus is disturbed during reperfusion.