Objective: To observe the effect of salvianolic acid A on heart rate variability (HRV) and myocardial injury in rats with myocardial ischemia-reperfusion injury.
Methods: 60 SD rats were randomly divided into 6 groups, namely sham operation group, MI/RI model group, SAA low, medium and high (0.5 mg/kg, 1 mg/kg and 2 mg/kg) dose groups and Positive control (2 mg/kg diltiazem) group, 10 mice in each group. The MI/RI rat model was established by ligating the left anterior descending coronary artery in rats, and the corresponding drugs were administered before the ligation. During the observation and analysis of ECG J-point and HRV changes, and double staining with Evans blue (evans blue, EB) and 2,3,5-triphenyltetrazolium chloride (TTC) after reperfusion The myocardial infarction area was determined by the method, and plasma aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and its isoenzyme (CK-MB), superoxide dismutase (SOD), Dialdehyde (MDA) and Nitric Oxide (NO) content.
RESULTS: Compared with MI/RI model group, SAA low, medium and high dose groups and diltiazem group could significantly reduce the ∑-J value and the average value of J point in reperfusion period rats (P<0.05, P<0.01). ), reduced myocardial infarction size and inhibited the increase of AST, CK-MB and CK activity (P<0.05, P<0.01); significantly increased the standard deviation of RR intervals (SDNN), the square of the difference between adjacent RR intervals Root mean square (RMSSD) of sum, HRV trigonometric function (tr.Ind) and high frequency (HFnu), and decreased low frequency (LFnu) and LF/HF ratio (P<0.05, P<0.01), but also significantly increased NO content and decreased MDA content (P<0.05).
Conclusion: Salvianolic acid can increase HRV and reduce myocardial infarction size, and its mechanism is related to the antioxidant effect of salvianolic acid A.