Fig. 3.

Contractile properties of pediatric skinned cardiomyocytes. A: pCa₅₀ of pediatric dilated cardiomyopathy (DCM) cardiomyocytes (5.70 ± 0.0291) is significantly increased (P = 0.0073) compared with that of pediatric nonfailing (NF) cardiomyocytes (5.59 ± 0.0271). B: pCa₅₀ of NF cardiomyocytes is unchanged with acute protein kinase A (PKA) treatment (NF+PKA 5.53 ± 0.0281), whereas pCa₅₀ of DCM cardiomyocytes decreases (P = 0.0043) with acute PKA treatment (DCM+PKA 5.46 ± 0.0430). C: median peak tension generation is similar between NF [32.8, interquartile range (IQR) 21.5–49.2] and DCM (29.7, IQR 21.6–47.0) cardiomyocytes. D: no significant changes in peak tension were present in NF or DCM samples treated with PKA. E: cooperativity, as represented by the Hill coefficient (n_H), is decreased (P = 0.0425) in DCM (1.56, IQR 1.31–1.94) compared with NF (1.94, IQR 1.36–2.86). F: acute PKA treatment did not significantly alter cooperativity in either DCM (2.14, IQR 1.31–2.61) or NF (2.19, IQR 1.38–3.20). NF: no. of subjects (N) = 8, no. of cardiomyocytes (n) = 33; NF+PKA: N = 8, n = 29; DCM: N = 8, n = 26; DCM+PKA: N = 8, n = 26. PDE3i, chronically treated with a phosphodiesterase 3 inhibitor before explant.