Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus

Author:

Wu Shengbing1,Cao Jian2,Zhang Tianning3,Zhou Yiping4,Wang Keming4,Zhu Guoqi1,Zhou Meiqi14

Affiliation:

1. Key Laboratory of Xin’an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei 230038, China

2. Department of Science and Technology, Anhui University of Chinese Medicine, Hefei, China

3. Anhui No. 2 Province People’s Hospital, Hefei, China

4. Institute of Acupuncture and Meridian, Anhui University of Chinese Medicine, Qianjiang Road 1, Hefei 230012, China

Abstract

Mechanisms for electroacupuncture (EA) in disease treatments are still enigmatic. Here, we studied whether hippocampus was involved in the protection of EA stimulation on myocardial ischemia injury. Acute myocardial ischemia (AMI) model was produced. EA stimulation at heart meridian from Shenmen (HT7) to Tongli (HT5) was applied to rats 3 times a day for continuous three days. Coronary occlusion related tachycardia and hypotension, indicated by heart rate, mean arterial pressure, and rate pressure product, were apparently impaired after AMI injury. By contrast, EA stimulating could ameliorate the impairments of heart function (P<0.05). Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA. Neuronal activity in CA1 area was affected by AMI. As evidenced, cell counts, cell types, and frequency of the discharged neurons were facilitated after AMI, while EA stimulation attenuated the abnormalities. Furthermore, c-Fos expression was significantly facilitated in CA1 area after AMI, which was reduced by EA stimulation. Correlations were established between c-Fos expression and cell counts of discharged neurons, as well as between heart function and cell counts of discharged neurons. Taken together, EA stimulation at heart meridian protects against heart dysfunction induced by AMI possibly through suppressing the neuronal activity in CA1 region.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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