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Background.Enhanced recovery after cardioplegic arrest has been observed in rat hearts with hypertrophy induced by hemodynamic overload. We hypothesize that this is related to altered characteristics of hypertrophied myocardium—reflected by increased V3 isomyosin and glycolytic potential—other than increased left ventricular mass.
Materials and methods. Isolated hearts from age-matched nonoperated and sham-operated control rats and from aortic-banded, hyperthyroid, and hypothyroid rats—groups in which hypertrophy and V3 as a percentage of left ventricular myosin vary independently—underwent 2 h of multidose cardioplegic arrest at 8°C followed by reperfusion at 37°C. Left ventricular V3 isomyosin was evaluated after separation by gel electrophoresis.
Results. Moderate left ventricular hypertrophy was produced by aortic banding or hyperthyroidism and atrophy by hypothyroidism. V3 isomyosin was increased in banded (28%) and hypothyroid (75%) rats compared to control (12%) and hyperthyroid rats (7%). Myocardial glycogen content closely paralleled %V3. At 30 min of working reperfusion, functional recovery (assessed as percentage prearrest cardiac output) was 66 ± 4 and 68 ± 5% in control and hyperthyroid hearts and 81 ± 2 and 80 ± 5% in hearts from banded and hypothyroid rats (each P < 0.05 vs controls), respectively. At 30 min, hearts from banded and hypothyroid rats were also more efficient (as indexed by cardiac output at constant mean aortic pressure/myocardial oxygen consumption) than control and hyperthyroid hearts.
Conclusions. The data suggest that recovery is related not to increased mass but to other changes in overload hypertrophy. Increased percentage V3 isomyosin and glycogen reflect these changes and may themselves contribute to improved functional recovery after cardioplegic arrest, as may increased postischemic efficiency.
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