| Objection: This study was to evaluate the relationship between calcium leak and ca/calmodulin-dependent protein kinase-II (CaMKⅡ) and protein kinase A (PKA) abundance and activity in myocytes of Rabbits with heart failure,which were established by volume overload plus pressure overload.Methods: (1)30 rabbits were divided into two groups:sham rabbits(controls, n=15) and rabbits with heart failure (HF,n=15).Heart failure models were established by volume plus pressure overload. (2)Cardiac functions were measured via catheterization and echocardiography. (3)Calcium leak assay was determined using fluorescence spectroscopy. (4)CaMKⅡand PKA abundance and activity were determined by Western blot analysis and [γ-32P] ATP-binding assays respectively.Results:(1)Cardiac function: compared to sham-operated rabbits, LVEDP (mmHg: -6.00±3.70 vs 25.10±4.33) in rabbits with heart failure were significantly increased (P<0.05) while EF (%:72.35±3.27 vs 43.67±7.12) were significantly decreased(P<0.05).(2)Calcium leak of Sarcoplasmic Reticular: Compared to Sham rabbits, after the treatment with Ruthenium Red,calcium reuptake of SR (nmol/l:98.64±20.15 vs 221.67±19.32) in failing rabbits was significantly increased(P<0.01).(3)Protein kinase expression and activity: compared to sham-operated rabbits, protein abundance of CaMKII (RCaMKII/actin:0.78±0.20 vs 1.24±0.34) and activity (pmol·min-1·μg-1:2.20±0.14 vs 4.12±0.19) were markedly increased(P <0. 05), whereas protein abundance of PKA (RPKA/actin:0.89±0.12 vs 0.59±0.21) and activity (pmol·min-1·μg-1:1.83±0.07 vs 1.01±0.03) were significantly decreased(P<0.05). Conclusion: (1)Animal models of heart failure were established by volume overload plus pressure overload in rabbits successfully.(2)Calcium leak was increased in failing rabbits obviously.(3)The SR calcium leak in heart failing rabbits was increased which was maybe due to increased CaMKⅡabundance and activity activating RyR2 excessively in this experiment. |
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