OBJECTIVE: To study the effects of different doses of tetramethylpyrazine on injury and calcium overload in myocardial cells of diastole heart failure rat model. METHOD: Diastole heart failure model was established by the coarctation of abdominal aorta. 4 weeks after operation, forty rats with DHF were divided into four groups randomly as follows, model (physiological saline 2 mL), tetramethylpyrazine (40 mg x kg(-1) x d(-1)), tetramethylpyrazine (20 mg x kg(-1) x d(-1)), tetramethylpyrazine (10 mg x kg(-1) x d(-1)), with 10 rats for each group (n = 10), and 10 sham operation rats was taken as control (physiological saline, 2 mL). After 4 weeks administration, cardiac function was determined by catheter. The changes of myocardial ultrastructure were investigated by means of transmission electron microscope. [Ca2+ ]i was measured by laser scanning confocal microscope [LSCM]. Ca(2+) -ATPase activity of mitochondrion was measured by the method of enzymatic reaction chromatometry. RESULT: Compared with the control group, the rats of operation group have no significant changes on left ventricular systolic pressure (LVSP) and maximal rising rate of ventricular pressure (+dp/dt(max)), but left ventricular end diastolic pressure (LVEDP) increased markedly, maximal delining rate of ventricular pressure (-dp/dt(max)) decreased significantly, left ventricular relax time constant quantity (T) markedly extended, myocardial pathology injured markedly, [Ca2+]i in cardiocyte increased markedly and the Ca(2+) -ATPase activity of myocardial mitochondria decreased significantly in the model group. After 4 weeks administration, compared with the model group, LVEDP decreased significantly, -dp/dt(max) increased markedly, T markedly shortened, myocardial ultrastructure damage were significantly reduced, fluorescent value decreased and Ca(2+) -ATPase activity of mitochondrion increased significantly in TMP low-dose group and mid-dose group. CONCLUSION: Low dosage of TMP can reduced myocardial pathology injury, increased Ca(2+)-ATPase activity of myocardial mitochondria, improve cardiac function and [Ca2+]i in cardiocyte and antagonise calcium overload of rats with DHF.
OBJECTIVE: To study the effects of different doses of tetramethylpyrazine on injury and calcium overload in myocardial cells of diastole heart failurerat model. METHOD:Diastole heart failure model was established by the coarctation of abdominal aorta. 4 weeks after operation, forty rats with DHF were divided into four groups randomly as follows, model (physiological saline 2 mL), tetramethylpyrazine (40 mg x kg(-1) x d(-1)), tetramethylpyrazine (20 mg x kg(-1) x d(-1)), tetramethylpyrazine (10 mg x kg(-1) x d(-1)), with 10 rats for each group (n = 10), and 10 sham operation rats was taken as control (physiological saline, 2 mL). After 4 weeks administration, cardiac function was determined by catheter. The changes of myocardial ultrastructure were investigated by means of transmission electron microscope. [Ca2+ ]i was measured by laser scanning confocal microscope [LSCM]. Ca(2+) -ATPase activity of mitochondrion was measured by the method of enzymatic reaction chromatometry. RESULT: Compared with the control group, the rats of operation group have no significant changes on left ventricular systolic pressure (LVSP) and maximal rising rate of ventricular pressure (+dp/dt(max)), but left ventricular end diastolic pressure (LVEDP) increased markedly, maximal delining rate of ventricular pressure (-dp/dt(max)) decreased significantly, left ventricular relax time constant quantity (T) markedly extended, myocardial pathology injured markedly, [Ca2+]i in cardiocyte increased markedly and the Ca(2+) -ATPase activity of myocardial mitochondria decreased significantly in the model group. After 4 weeks administration, compared with the model group, LVEDP decreased significantly, -dp/dt(max) increased markedly, T markedly shortened, myocardial ultrastructure damage were significantly reduced, fluorescent value decreased and Ca(2+) -ATPase activity of mitochondrion increased significantly in TMP low-dose group and mid-dose group. CONCLUSION: Low dosage of TMP can reduced myocardial pathology injury, increased Ca(2+)-ATPase activity of myocardial mitochondria, improve cardiac function and [Ca2+]i in cardiocyte and antagonise calcium overload of rats with DHF.