Effect of Point Neiguan(PC6) Electroacupuncture Pretreatment on NO, NOS and Mitochondrial Membrane Potential in Rats with Myocardial Ischemia/Reperfusion Injury / 上海针灸杂志

ABSTRACT

Objective To explore the effect of point Neiguan(PC6) electroacupuncture pretreatment on nitric oxide (NO), nitric oxide synthase (NOS) and mitochondrial membrane potential by determining NO, NOS and mitochondrial membrane potential in rats with myocardial ischemia/reperfusion injury (MIRI).Method Forty male SD rats were randomized to sham operation, ischemia/reperfusion model, point Neiguan electroacupuncture and point Huantiao(GB30) electroacupuncture groups, 10 rats each. The model was made by coronary artery ligation. Before model making, electroacupuncture was given to the point Neiguan electroacupuncture and point Huantiao electroacupuncture groups, 20 min/d for a total of 7 d. T wave value in ECG leadⅡ was measured before and after model making. Myocardial pathomorphological changes were examined by HE staining. Serum NO and NOS contents were measured by a colorimetric nitrate reductase assay. Cardiomyocyte mitochondrial membrane potential was determined by fluorescence techniques.Result Serum NO and NOS contents and mitochondrial membrane potential decreased significantly in the model group compared with the sham operation group (P<0.05). Serum NO and NOS contents increased significantly in the point Neiguan electroacupuncture group compared with the model, sham operation and point Huantiao electroacupuncture groups (P<0.01,P<0.05). Mitochondrial membrane potential increased significantly in the point Neiguan electroacupuncture group compared with the model, point Huantiao electroacupuncture and sham operation groups (P<0.01,P<0.05). There was no statistically significant difference in mitochondrial membrane potential between the model and point Huantiao electroacupuncture groups (P>0.05). Conclusion Point Neiguan electroacupuncture pretreatment has a preventive protecting effect on MIRI rats. It produces a protecting effect on myocardium by increasing the NO content, strengthening NOS activity, reducing a decrease in cardiomyocyte mitochondrial membrane potential and inhibiting apoptosis.