OBJECTIVE: To explore the changes of expression of uncoupling protein 2 (UCP2) in pressure overload induced failure myocardium in rats. METHODS: Male SD rats were randomized into 3 groups (n = 15 each): abdominal aorta constriction (AC) 20 weeks group (H20w group), sham operation group (SH20w group) and normal control group (N group). Twenty weeks later, myocardial function was evaluated by echocardiography and hemodynamic measurements. Mitochondria in ventricular tissue were isolated by centrifugation. Adenine nucleotide pools (ATP, ADP, AMP, PCr) in myocardium were measured by high performance liquid chromatography. The expression of UCP2 in mitochondria was detected by PT-PCR and Western blot analysis. RESULTS: Myocardial function was significantly decreased 20 weeks post-AC compared to SH20w group and N group. Myocardial ATP, ADP, AMP and PCr contents were also significantly decreased in H20w group than the other 2 control groups. The expression of UCP2 in myocardial mitochondria was significantly increased in H20w group and negatively correlated with ATP contents (r = -0.929, P < 0.01). CONCLUSIONS: The expression of UCP2 was upregulated in pressure overload induced failure heart and might be responsible for decreased myocardial adenine nucleotide and energy metabolism disturbance in this model.
OBJECTIVE: To explore the changes of expression of uncoupling protein 2 (UCP2) in pressure overload induced failure myocardium in rats. METHODS: Male SD rats were randomized into 3 groups (n = 15 each): abdominal aorta constriction (AC) 20 weeks group (H20w group), sham operation group (SH20w group) and normal control group (N group). Twenty weeks later, myocardial function was evaluated by echocardiography and hemodynamic measurements. Mitochondria in ventricular tissue were isolated by centrifugation. Adenine nucleotide pools (ATP, ADP, AMP, PCr) in myocardium were measured by high performance liquid chromatography. The expression of UCP2 in mitochondria was detected by PT-PCR and Western blot analysis. RESULTS: Myocardial function was significantly decreased 20 weeks post-AC compared to SH20w group and N group. Myocardial ATP, ADP, AMP and PCr contents were also significantly decreased in H20w group than the other 2 control groups. The expression of UCP2 in myocardial mitochondria was significantly increased in H20w group and negatively correlated with ATP contents (r = -0.929, P < 0.01). CONCLUSIONS: The expression of UCP2 was upregulated in pressure overload induced failure heart and might be responsible for decreased myocardial adenine nucleotide and energy metabolism disturbance in this model.