Abstract

The progression of DCM has been assumed to be a homogenous process for both the RV and LV. However, this assumption has never been tested. Accordingly, we measured myocyte contractile performance (velocity of shortening, VELSHORT; percent shortening, PERSHORT) at baseline (BASE) and after β -adrenergic receptor stimulation ( β AR, 25 nM isoproterenol) of isolated myocytes taken from the RV and LV of 5 pigs with pacing induced DCM (240 bpm, 3 weeks) and 5 control pigs (CON). RV and LV mass/body weight (MASS) and myocyte length and cross-sectional area (CSA) were also determined. CON-RV CON-LV DCM-RV DCM-LV VELSHORT-BASE ( μ m/s) 90 ± 5 + 50 ± 1 48 ± 2 * , + 32 ± 1 * VELSHORT- β AR ( μ m/s) 206 ± 8 + 150 ± 5 123 ± 8 * 111 ± 9 * PERSHORT-BASE (%) 5.8 ± 0.2 + 4.6 ± 0.1 3.1 ± 0.1 * , + 2.2 ± 0.1 * PERSHORT- β AR (%) 11.5 ± 0.3 + 10.2 ± 0.3 59 ± 0.3 * 5.2 ± 0.4 * Length ( μ m) 150 ± 2 + 137 ± 1 179 ± 2 * , + 173 ± 2 * CSA ( μ m 2 ) 176 ± 4 + 362 ± 8 232 ± 4 * , + 292 ± 5 * Mass (gm/kg) 0.8 ± 0.1 + 2.8 ± 0.1 1.6 ± 0.1 * , + 2.9 ± 0.2 + p < 0.05 vs LV * p < 005 vS CON In controls, RV myocytes were longer and had a smaller CSA, but enhanced contractile performance at baseline and with β -adrenergic stimulation. With DCM, no LV hypertrophy occurred. In contrast, RV chamber and cellular hypertrophy occurred and was associated with a persistent increase of RV myocyte baseline contractile function. This study demonstrated, for the first time, that differences in RV and LV myocyte function and β -adrenergic responsiveness exist in normal and DCM states. More importantly, a disparity in RV and LV myocyte growth with DCM occurred. Thus, in this model of DCM, RV and LV growth and changes in contractile performance are not a homogenous process, and suggest that inherent differences exist in the response of RV and LV myocytes to stress.

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