Figure 3. Percent change from baseline for myocyte velocity of shortening in normothermic (control) myocytes and myocytes exposed to hypothermic cardioplegic arrest and rewarming in the presence of 8 mM Calcium2+ or 10 nM isoproterenol. Eight millimoles Calcium2+ and 10 nM isoproterenol represent optimal concentrations for enhancement of contractile function in normothermic, control myocytes. The percent change in myocyte velocity of shortening was significantly lower after hypothermic cardioplegic arrest compared to control in the presence of 8 mM Calcium2+. In contrast, the percent change from baseline in the presence of 10 nM isoproterenol was not significantly different between the normothermic (control) and hypothermic cardioplegic arrested and rewarmed myocytes (*P < 0.05 vs. control).

Figure 3. Percent change from baseline for myocyte velocity of shortening in normothermic (control) myocytes and myocytes exposed to hypothermic cardioplegic arrest and rewarming in the presence of 8 mM Calcium2+ or 10 nM isoproterenol. Eight millimoles Calcium2+ and 10 nM isoproterenol represent optimal concentrations for enhancement of contractile function in normothermic, control myocytes. The percent change in myocyte velocity of shortening was significantly lower after hypothermic cardioplegic arrest compared to control in the presence of 8 mM Calcium2+. In contrast, the percent change from baseline in the presence of 10 nM isoproterenol was not significantly different between the normothermic (control) and hypothermic cardioplegic arrested and rewarmed myocytes (*P < 0.05 vs. control).

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