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1 Institute of Experimental Surgery and 2 Clinic of Thoracic and Cardiovascular Surgery, Heinrich-Heine-University Düsseldorf, D-40225 Düsseldorf, Germany
Myocardial
O2 consumption
(M
O2) in stunned myocardium
is relatively high compared with the reduced ventricular function. The
mechanism of this "oxygen paradox" could occur at different levels: basal metabolism, excitation-contraction coupling, and energy
production. In one previously reported series on 12 isolated, blood-perfused rabbit hearts, left ventricular systolic and diastolic function in stunned myocardium were significantly decreased compared with control, whereas total
M
O2 was not. The
M
O2 for the unloaded contraction was overproportionately high for the decreased function in
stunned myocardium, and contractile efficiency was clearly deteriorated. To assess whether the basal metabolism specifically is
elevated in stunned myocardium, a second series
(n =14) with a similar protocol was
performed in this study. Basal
M
O2 after KCl arrest (0.5 ± 0.3 ml · min
1 · 100 g
1) was significantly
lower than that measured after KCl arrest (1.2 ± 0.5 ml · min
1 · 100 g
1) in an additional
series on nonischemic hearts (n = 8).
Our conclusion is that basal
M
O2 in stunned myocardium
is not elevated. Thus this
O2-consuming portion of total
M
O2 is not responsible for the inefficiency in stunned myocardium. Instead, a "metabolic stunning" occurs at the level of both excitation-contraction
coupling and force development by the contractile apparatus.
myocardial stunning; isolated heart; rabbit
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