Figure 7.

Reduced contractility and myofilament Ca²⁺ sensitization in Cpa3^cre/+ mice after infarction. (A) Depressed left ventricular cardiomyocyte cell shortening (%) of Cpa3^cre/+-derived intact cardiomyocytes versus WT cardiomyocytes in response to field stimulation (1, 2, and 4 Hz; n = 30–50, two independent experiments). *, P < 0.05; **, P < 0.01, Kruskal–Wallis and Dunn’s post hoc test for comparisons between groups. (B) Both contraction and relaxation kinetics were significantly reduced in Cpa3^cre/+-derived cardiomyocytes versus WT cardiomyocytes (n = 30–50, two independent experiments). *, P < 0.05, Kruskal–Wallis and Dunn’s post hoc test for comparisons between groups. (C) MC deficiency had no effect on Ca²⁺ transient peak (n = 30–50, two independent experiments). (D) SR Ca²⁺ content in response to 1-Hz electric stimulation and after caffeine (10 mmol/l) was similar in both WT and Cpa3^cre/+-derived cardiomyocytes (n = 30–50, two independent experiments). (E) Force–calcium fitted curves reflecting Ca²⁺ responsiveness of left ventricle peri-infarcted skinned myocytes from WT and Cpa3^cre/+ mice after sham operation or MI. Reduced Ca²⁺ sensitivity in both WT and Cpa3^cre/+-derived skinned myocytes in response to MI with a shift to the right in Cpa3^cre/+-derived myocytes versus WT (n = 5–8, two independent experiments). (F and G) F_max was not altered between WT and Cpa3^cre/+-derived myocytes (F), but MC deficiency caused Ca²⁺ desensitization with a significant increase in EC₅₀ (G; n = 5–8, two independent experiments). **, P < 0.01, Kruskal–Wallis and Dunn’s post hoc test for comparisons between groups. (H) No difference in Hill coefficient as a measure of Ca²⁺ cooperativity (n = 5–8, two independent experiments). All values are presented as mean ± SEM. ns, not significant; Sham, sham-operated animals; SR, sarcoplasmic reticulum.