[Electroacupuncture at "Zusanli" (ST 36) Alleviates Myocardium Damage in Intestinal Ischemia-reperfusion Rats by Up-regulating Periphery Dopamine Level].

OBJECTIVE

To observe the effect of electroacupuncture (EA) of "Zusanli" (ST 36) on myocardium ischemic damage following intestinal ischemia-reperfusion (I/R) in rats.

METHODS

Thirty SD rats were randomly divided into five groups:sham, I/R-1 h, I/R-4 h, EA-I/R-1 h and EA-I/R-4 h (n=6 in each group). The intestinal I/R model was established by occlusion of the superior mesenteric artery. EA (2 Hz/100 Hz, 2-3 mA) was applied to bilateral ST 36 for 30 min. In rats of the sham group, only the stomach was opened. Plasma dopamine (DA) and tumor necrosis factor (TNF)-α contents, and myocardial myeloperoxidase (MPO) activity and methane dicarboxylic aldehyde (MDA) content were assayed using ELISA, and plasma creastine kinase isoenzyme (CK-MB) and lactate dehydrogenese (LDH) activities were detected using a fully biochemical analyser. Myocardial pathological changes were observed under microscope after H.E. staining.

RESULTS

Compared with the sham group, plasma DA content was significantly decreased in both I/R-1 h and I/R-4 h groups, while plasma TNF-α content and CK-MB and LDH activities, and myocardial MPO activity and MDA content in both I/R-1 h and I/R-4 h groups were obviously increased (P<0.05). After EA, the decreased plasma DA and the increased plasma TNF-α contents and the increased plasma CK-MB and LDH and myocardial MPO activities and MDA contents in the EA-I/R-1 h and EA-I/R-4 h groups were reversed (P<0.05). The inhibitory rates of EA on myocardial MDA content and MPO activity were 9% and 13% in the EA-I/R-1 h group and 30% and 15% in the EA-I/R-4 h group, respectively, suggesting a better protective effect of EA intervention on myocardium in the EA-I/R-4 h group.

CONCLUSIONS

EA of ST 36 has a better protective action on myocardium in intestinal I/R injury rats, which may be related to its effects in up-regulating plasma DA level and down-regulating circulating pro-inflammatory factor TNF-α content, and reducing myocardial oxygen free radicals.