Ca⁺²/Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction

Figure 3

Mechanical property of adult rat cardiomyocytes maintained for 12 hours in a serum-free medium with normal glucose (NG: 5.5 mM) or high glucose (HG: 25.5 mM) in the absence or presence of high extracellular Ca²⁺ (Hi-Ca, 2.7 mM) in the contractile buffer. An extracellular Ca²⁺ concentration of 1.0 mM was used as the normal low Ca²⁺ (LoCa) environment. (a) Resting cell length (b) peak shortening (PS) amplitude normalized to cell length; (c) Maximal velocity of shortening (+dL/dt); (d) Maximal velocity of relengthening (−dL/dt), (e) time to PS (TPS), and (f) time to 90% relengthening (TR₉₀). Mean ± SEM, 𝑛=38–42 cells per group, *𝑃<0.05 versus NG-LoCa group, ^#𝑃<0.05 versus HG-LoCa group.

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