Abstract
BackgroundSympathetic overactivation and inflammation are two major mediators to post-myocardial ischemia-reperfusion (I/R)-induced ventricular arrhythmia (VA). The vicious cycle between microglia and sympathetic activation plays an important role in sympathetic hyperactivity related to cardiovascular diseases. Recently, studies have shown that microglial activation might be attenuated by light-emitting diode (LED) therapy. Therefore, we hypothesized that LED therapy might protect against myocardial I/R-induced VAs by attenuating microglial and sympathetic activation.MethodsThirty-six male anesthetized rats were randomized into four groups: control group (n = 6), LED group (n = 6), I/R group (n = 12), and LED+I/R group (n = 12). I/R was generated by left anterior descending artery occlusion for 30 min followed by 3 h reperfusion. ECG and left stellate ganglion (LSG) neural activity were recorded continuously. After 3 h reperfusion, a programmed stimulation protocol was conducted to test the inducibility of VA. Furthermore, we extracted the brain tissue to examine the microglial activation, and the peri-ischemic myocardium to examine the expression of NGF and inflammatory cytokines (IL-1β, IL-18, IL-6, and TNF-α).ResultsAs compared to the I/R group, LED illumination significantly inhibited the LSG neural activity (P < 0.01) and reduced the inducibility of VAs (arrhythmia score 4.417 ± 0.358 vs. 3 ± 0.3257, P < 0.01) in the LED+I/R group. Furthermore, LED significantly attenuated microglial activation and downregulated the expression of inflammatory cytokines and NGF in the peri-infarct myocardium.ConclusionsLED therapy may protect against myocardial I/R-induced VAs by central and peripheral neuro-immune regulation.
Highlights
Restoring blood flow to the ischemic myocardium by primary percutaneous coronary intervention or thrombolytic therapy is the most effective strategy for improving the patients’ clinical outcome after acute myocardial infarction (AMI)
All these implicated that vicious cycle between sympathetic activation and microglial activation in the paraventricular nucleus (PVN) might exist in neuro-immune activation related diseases and that microglial intervention might be a novel target for therapy
Compared to the I/R group, the I/R-induced increase of left stellate ganglion (LSG) neural activity was significantly reduced by light-emitting diode (LED) illumination in both frequency and amplitude in the LED+I/R group
Summary
Restoring blood flow to the ischemic myocardium by primary percutaneous coronary intervention or thrombolytic therapy is the most effective strategy for improving the patients’ clinical outcome after acute myocardial infarction (AMI). Myocardial ischemia-reperfusion (I/R) injury, including I/R-induced ventricular arrhythmia (VA), It has been reported that the microglial activation in the hypothalamic paraventricular nucleus (PVN), indicating inflammation in this nucleus, was involved in many cardiovascular diseases related with neuroimmune dysfunction, such as AMI [5, 6] and hypertension [7]. Previous studies demonstrated that attenuating microglial activation with minocycline might decrease blood pressure, inhibit inflammatory response [7], and improve cardiac function post-AMI [8]. All these implicated that vicious cycle between sympathetic activation and microglial activation in the PVN might exist in neuro-immune activation related diseases and that microglial intervention might be a novel target for therapy. We hypothesized that LED therapy might protect against myocardial I/R-induced VAs by attenuating microglial and sympathetic activation
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