目的 :探讨电针的抗心肌缺血机制

进一步研究经脉脏腑相关理论。方法 :采用大剂量异丙肾上腺素 ( 1 0 0mg/kg)腹腔注射建立急性心肌缺血实验模型

观察电针“心俞”、“厥阴俞”对血清中肌酸激酶 (CK)、超氧化物歧化酶 (SOD)、丙二醛 (MDA)、血浆中降钙素基因相关肽 (CGRP)和内皮素 (ET)含量的影响。结果 :电针“心俞”、“厥阴俞”能降低血清CK含量 (P <0 .0 5)

和MDA含量 (P <0 .0 1 )

提高血清SOD含量 (P <0 .0 0 1 )和血浆CGRP/ET水平 (P <0 .0 0 1 )。结论 :电针对大鼠急性心肌缺血具有预防和治疗作用

可以保护心肌

改善心肌缺血损伤

进一步证实了经脉脏腑相关理论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(P<0.01～0.001)

but there was no significant difference between EA and control group (P>0.05)

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 (P<0.05～0.01) but no apparent difference was found between model group and control group (P>0.05). 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 (P>0.05)in spite of being higher in EA group. Plasma CGRP of model group was significantly lower than those of control group (P<0.001)

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(P<0.01); but there was no significant difference between EA group and control group (P>0.05)

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 (P>0.05)

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.