Electroacupuncture preconditioning alleviates myocardial ischemia-reperfusion injury through the hypothalamic...

To explore whether the paraventricular nucleus (PVN) participates in regulation of the anti-myocardial ischemia-reperfusion injury (MIRI) effect of electroacupuncture (EA) and whether this is achieved through the PVN-interposed nucleus (IN) neural pathway.

The modeling method of myocardial ischemia reperfusion injury was achieved by ligating the left anterior descending coronary artery in Sprague-Dawley rats. We used the Powerlab multi-channel physiological recorder system to record electro-cardiograms and analyze the changes in ST segment displacement; 2,3,5-Triphenyltetrazolium chloride staining was used to observe the percentage of myocardial infarction areas. Detecting cardiac troponin I (cTnI), lactate dehydrogenase (LDH) in serum was done with an enzyme-linked immunosorbent assay kit. Morphological changes in the myocardium were detected in each group with hematoxylin-eosin staining of paraffin sections. Detection of c-fos protein expression in the PVN of the hypothalamus was done with the immune-ofluorescence method. The Plexon multi-channel acquisition system recorded PVN neuron discharges and local field potentials in each group of rats. Offline Sorter software was used for cluster analysis. Neuro Explorer software was used to perform autocorrelation, raster and frequency characteristics and spectral energy analysis of neuron signals in each group.

Compared with the MIRI model group, the areas of myocardial infarction in the EA group were significantly reduced; the expression of cTnI, LDH in serum was decreased significantly. The firing frequency of pyramidal cells in the PVN was significantly increased and the spectrum energy map showed energy was reduced, c-fos expression in PVN was reduced, this indicated that neuronal activity in the PVN participates in the effect of EA improving myocardial injury. In addition, we used the kainic acid method to lesion the IN and observed that the effect of EA was weakened. For example, the area of myocardial infarction of lesion IN + EA group in rats was significantly increased compared with that resulting from EA group, the expression of cTnI, LDH in serum was significantly increased, the firing frequency of pyramidal cells in the PVN was significantly reduced. A spectral energy diagram shows that the energy after damage was higher than that of EA group. At the same time, the expression of c-fos in the PVN increased again.

Our results indicated that the PVN-IN nerve pathway may participate as an effective pathway of EA to improve the effect of myocardial injury.