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

Figure 2

Mechanical property of adult rat cardiomyocytes cultured 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 the glycation inhibitor aminoguanidine (1 mM) or the translation inhibitor cycloheximide (60 μm). DMSO was used as a solvent with a final concentration less than 0.5%. (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=22–29 cells per group, *𝑃<0.05 versus NG group, ^#𝑃<0.05 versus HG group.

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