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Figure 4 (A and B) Representative traces of the sodium-calcium exchange current elicited by voltage ramp in a myocyte from a failing placebo-treated animal (A) and a failing furosemide-treated animal (B). Basal currents are seen in black, and the current in the same cell after stimulation with 2 µM isoproterenol (ISO) are presented in red. (C) Comparison of mean ± SEM peak outward sodium-calcium exchanger currents elicited from myocytes from nonfailing controls (yellow, n = 42 cells from 11 pigs), failing placebo-treated (red, n = 40 cells from 8 pigs), and furosemide-treated animals (purple, n = 50 cells from 9 pigs). Heart failure was associated with a significantly greater peak current, but furosemide use was associated with significantly greater current compared with placebo (*different compared with both failure groups, p < 0.05; #different from placebo cells, p < 0.05). (D) Comparison of mean ± SEM ratio of peak outward sodium-calcium exchanger currents elicited in response to ISO divided by basal current from failing myocytes from placebo- and furosemide-treated animals. Furosemide use was associated with significantly less inducible current compared with placebo and nonfailing controls, consistent with a reduction in responsiveness to beta-adrenergic stimulation (*different compared with both failure groups, p < 0.05; #different from placebo cells, p < 0.05).
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