Effect of electroacupuncture on porcine cardiac excitability induced by left stellate ganglion stimulation.

Auton Neurosci

Department of Anesthesiology, University of California Los Angeles, CA, United States; Department of Medicine, University of California, Irvine, CA, United States. Electronic address:

Published: September 2018

Augmentation of cardiac sympathetic tone has been shown to induce ventricular arrhythmias. Acupuncture has been clinically used to treat hypertension, angina pectoris, and atrial arrhythmias. However, the effects of acupuncture on ventricular electrophysiology and autonomic tone remain unknown. We hypothesized that acupuncture attenuates cardiac excitability and corrects the imbalance of autonomic tone during sympathetic hyperactivity. Fourteen Yorkshire pigs were randomized to electroacupuncture (EA, 2 Hz, 0.3-0.5 mA, 0.5 ms duration) or control (without EA) groups. Animals were sedated with terazol. General anesthesia consisted of isoflurane and fentanyl during surgical preparation and was transitioned to α-chloralose during experimental protocols. Through a median sternotomy, the heart was exposed and fitted with an elastic epicardial 56-electrode sock. Cardiac excitability was measured via activation recovery interval (ARI) and dispersion of repolarization (DOR) while autonomic balance was evaluated by heart rate variability (HRV) power spectrum analysis at baseline and during left stellate ganglion stimulation (LSS) with and without EA delivered at P 5-6 acupoints. 30-min of EA did not alter the baseline ARI and DOR, but significantly suppressed cardiac excitability during LSS through attenuation of ARI shortening (EA 2.1 ± 0.3% vs. control 5.2 ± 0.7%, P < 0.05) and DOR (EA 74.3 ± 26.9% vs., control 110.1 ± 22.9%, P < 0.05). EA significantly attenuated the increase in LF/HF (EA 0.6 ± 0.1 vs. control 1.1 ± 0.2, P < 0.05). In conclusion, EA reduces the cardiac excitability induced by LSS through correction of cardiac sympathovagal balance. This study provides mechanistic insights underlying cardiac neuromodulation of EA during sympathoexcitation.

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http://dx.doi.org/10.1016/j.autneu.2018.05.005DOI Listing

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