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

Wu S, Cao J, Zhang T, Zhou Y, Wang K, Zhu G, Zhou M - Evid Based Complement Alternat Med (2015)

Bottom Line: Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA.Neuronal activity in CA1 area was affected by AMI.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.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei 230038, 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.

No MeSH data available.


Related in: MedlinePlus

Myocardial ischemia injury activates neuronal discharge, while being ameliorated by EA treatment. (a) Representative electrophysiological images from different groups. (b) Cell numbers and cell types for the discharged cells. (c) Discharge frequency in different groups. Data were presented as mean and SD. ∗∗P < 0.01 compared with sham control. ##P < 0.01 compared with model.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4499623&req=5

fig5: Myocardial ischemia injury activates neuronal discharge, while being ameliorated by EA treatment. (a) Representative electrophysiological images from different groups. (b) Cell numbers and cell types for the discharged cells. (c) Discharge frequency in different groups. Data were presented as mean and SD. ∗∗P < 0.01 compared with sham control. ##P < 0.01 compared with model.

Mentions: As hippocampus was involved in the protective effect of acupuncture on myocardial ischemia injury, we identified the potential effects of AMI injury or EA on hippocampal CA1 neuronal activity. Both cell types and frequency of discharged neurons were evaluated. Compared with sham-operated group, the types and numbers of the discharged cells in CA1 region were significantly increased in the AMI modeled rats (Figures 5(a) and 5(b)). EA stimulation significantly weakened the neuronal discharge in both cell types and cell numbers.


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

Wu S, Cao J, Zhang T, Zhou Y, Wang K, Zhu G, Zhou M - Evid Based Complement Alternat Med (2015)

Myocardial ischemia injury activates neuronal discharge, while being ameliorated by EA treatment. (a) Representative electrophysiological images from different groups. (b) Cell numbers and cell types for the discharged cells. (c) Discharge frequency in different groups. Data were presented as mean and SD. ∗∗P < 0.01 compared with sham control. ##P < 0.01 compared with model.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499623&req=5

fig5: Myocardial ischemia injury activates neuronal discharge, while being ameliorated by EA treatment. (a) Representative electrophysiological images from different groups. (b) Cell numbers and cell types for the discharged cells. (c) Discharge frequency in different groups. Data were presented as mean and SD. ∗∗P < 0.01 compared with sham control. ##P < 0.01 compared with model.
Mentions: As hippocampus was involved in the protective effect of acupuncture on myocardial ischemia injury, we identified the potential effects of AMI injury or EA on hippocampal CA1 neuronal activity. Both cell types and frequency of discharged neurons were evaluated. Compared with sham-operated group, the types and numbers of the discharged cells in CA1 region were significantly increased in the AMI modeled rats (Figures 5(a) and 5(b)). EA stimulation significantly weakened the neuronal discharge in both cell types and cell numbers.

Bottom Line: Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA.Neuronal activity in CA1 area was affected by AMI.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.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Xin'an Medicine, Ministry of Education, Anhui University of Chinese Medicine, Hefei 230038, 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.

No MeSH data available.


Related in: MedlinePlus