Effect of Electroacupuncture on Blood Free Radicals, ET and CGRP Contents in Rats with Acute Myocardial Ischemia

Objective: To probe into mechanisms of electroacupuncture (EA) in resisting myocardial ischemia (MI) and to study the relationship between Xinshu(B 15)and Jueyinshu(B 14)acupoints of the Bladder Channel and the heart. Methods: EA (300 μs pulse width; 2～20 Hz; 3.5～5 V) was applied to left Xinshu(B 15)and Jueyinshu(B 14)for 30 min. 32 Wistar rats were evenly and randomly divided into prevention EA group, EA group, model group and control group. MI was induced by intravenous injection of isoproterenol (ISO, 100 mg/kg). In EA-prevention group, EA was performed only one time 1 hr before injection of ISO. In EA group, EA was preformed at the moment of injection of ISO and given once again 12 hr later. In model group, only ISO was used, and in control group normal saline (5 mL/kg) was injected intravenously. Changes of serum superoxide dismutase(SOD)activity, serum malondialdehyde (MDA) and creatine kinase (CK) contents were assayed using colorimetric method, while plasma calcitonin gene-related peptide (CGRP) and endothelin(ET) contents were detected with radioimmunoassay. Results: After MI, serum CK levels in EA-prevention group and model group increased significantly in comparison with control group(P0.01～0.001), but there was no significant difference between EA and control group (P0.05), showing the effect of EA being superior to that of EA-prevention. Following EA, serum SOD in the aforementioned two EA groups increased significantly in comparison with control group (P0.05～0.01) but no apparent difference was found between model group and control group (P0.05). Serum MDA level of model group was significantly higher than those of two acupuncture groups and control group (P 0.01), but there was no significant difference between EA and control group (P0.05)in spite of being higher in EA group. Plasma CGRP of model group was significantly lower than those of control group (P0.001), suggesting an increase of CGRP after MI. After EA, CGRP levels in two EA groups increased moderately, being close to that of control group. Following MI, plasma ET elevated significantly in comparison with control group and EA group(P0.01); but there was no significant difference between EA group and control group (P0.05), suggesting a suppressive action of EA on ET release. In regard to CGRP/ET , there was no apparent difference between control group and EA group (P0.05), while there was no significant difference between EA and control group (P 0.05). Conclusion: EA can effectively inhibit MI-induced increase of serum CK, free radical oxidation and plasma ET levels and raise plasma CGRP content, that may be associated with the good curative and preventive effects of EA on ischemic myocardial injury.