ABSTRACT
<p><b>OBJECTIVE</b>To observe the maximal heart rate changes, atrioventricular (A-V) conduction block and atrial fibrillation (AF) inducibility in dogs with vagosympathetic trunk exposed to electromagnetic fields (EMFs).</p><p><b>METHODS</b>The vagosympathetic trunk of adult dogs was separated and exposed to EMFs 0.043 kHz (2.87 microG, n = 5) and to EMFs 2 kHz (0.34 microG, n = 6) for two to three hours. Simultaneously, the vagosympathetic trunk was stimulated with 20 Hz frequency and 1 - 8 V intensity for 0.1 ms. Heart rate, presence of A-V conduction block and AF inducibility were determined.</p><p><b>RESULTS</b>After 5-minutes exposure to EMFs 0.043 kHz (2.87 microG), the maximal heart rate decreased 29%, the voltage applied to vagosympathetic trunk required to induce A-V conduction block decreased by 60% in experimental group versus 5% increase in control group. This effect lasted 2 to 3 hours. While vagosympathetic trunk exposure to EMFs 2 kHz (0.34 microG) was associated with significant increase in the incidence of atrial premature beats, atrial tachycardia and AF, these effects could be blocked by propranolol and atropine.</p><p><b>CONCLUSIONS</b>Our results showed that 0.043 kHz (2.87 microG) EMFs exposure might reduce while 2 kHz (0.34 microG) EMFs exposure might increase AF inducibility. Our study thus suggested autonomic nervous system of dogs could be affected by EMFs exposure and 0.043 kHz (2.87 microG) EMFs exposure might be a novel option for AF prevention.</p>
Subject(s)
Animals , Dogs , Atrial Fibrillation , Heart Rate , Magnetics , Vagus NerveABSTRACT
<p><b>OBJECTIVE</b>To explore the efficacy of sequential ablation of epicardial fat pad on inducibility of atrial fibrillation (AF) evoked by stimulating vagus trunk.</p><p><b>METHODS</b>Eighteen adult mongrel dogs were randomly divided into 2 groups (n = 9 each): Group A underwent pre-ablation of sinus-atrial node fad pad (SANFP) and subsequent ablation of atria-ventricular node fad pad (AVNFP). Group B underwent pre-ablation of AVNFP and subsequent ablation of SANFP. AF was induced by high-frequency electrical stimulation of bilateral vagus trunks. The AF inducibility and effective refractory period (ERP) changes during vagus trunk stimulation were examined before and after ablation in atria and pulmonary veins.</p><p><b>RESULTS</b>(1) AF could be induced by vagus trunk stimulation and the incidence was higher during right vagus trunk (RVG) stimulation than left vagus trunk (LVG) stimulation [(60.0 ± 0.0)% vs (18.4 ± 22.1)%]. (2) SANFP ablation significantly attenuated AF inducibility with LVG stimulation and RVG stimulation at 2 V (decreased 67.0% and 72.0%, respectively). Subsequent AVNFP ablation after SANFP ablation further reduced AF inducibility with LVG and RVG stimulation at 2 V (decreased 100.0% and 95.5%, respectively). (3) AVNFP ablation (decreased 95.7% and 96.3%, respectively) and subsequent SANFP ablation after AVNFP ablation (decreased 98.0% and 100.0%, respectively) significantly attenuated AF inducibility with LVG stimulation and RVG stimulation at 2V. (4) Vagal stimulation induced ERP shortening was significantly attenuated by isolated SANFP ablation or AVNFP. Subsequent AVNFP ablation after SANFP induced significant ERP shortening in right atrial site compared with isolated SANFP ablation. However, changes of ERP shortening were similar between AVNFP ablation and subsequent SANFP ablation after AVNFP ablation.</p><p><b>CONCLUSIONS</b>Epicardial fat pad ablation reduced the AF inducibility and prolonged ERP of atria and pulmonary veins during vagus trunk stimulation. AVNFP, as the "integration centers" modulating the vagal innervation to the atria, may be the more effective target of ablation for treating AF.</p>
Subject(s)
Animals , Dogs , Adipose Tissue , Atrial Fibrillation , Catheter Ablation , Electric Stimulation , Sinoatrial Node , Vagus NerveABSTRACT
<p><b>OBJECTIVE</b>The study aimed to investigate the relationship between arrhythmia occurrence and nerve remodeling of thoracic spinal cord 1-5 nerves as well as myocardial electrophysiological remodeling in a metal stress rat model.</p><p><b>METHODS</b>Thirty SD rats (weight 180-250 g) were randomly divided into control group (n = 10), stress group (n = 10) and fluoxetine group (n = 10, 10 mg/kg i.p. for 3 weeks). Stress model (given by unpredicted chronic mild stress) was established according to Cronli's protocol. Following parameters were observed:(1) ECG waveform change and arrhythmias;(2) tissue field action potential duration (FAPD) of thoracic spinal cord 1-5 and cardiac tissue mapped by microelectrode arrays (MEA) technique;(3) myocardial growth-associated protein (GAP-43), tyrosine hydroxylase (TH), choline acetyltransferase (CHAT) distribution observed by immunofluorescence and confocal laser scanning microscope (LSCM).</p><p><b>RESULTS</b>Three weeks later: (1) The body weight, food intake, consumption of sugar water, the horizontal and vertical movement score, cleaning action of rats were significantly decreased, and fecal grains significantly increased, P-wave, P-R interval, QRS-wave and Q-T interval were significantly prolonged and heart rate was significantly reduced in stress group compared with control group (all P < 0.05). Incidence of ventricular premature beat was 80% in stress group and 0% in control group (P < 0.05). The FAPD of thoracic spinal cord 1-5 nerves [(144.25 ± 12.63)ms vs (79.56 ± 8.01)ms] and of cardiac tissue [LA(122.43 ± 19.34)ms vs (92.59 ± 7.61)ms, RA(149.89 ± 14.68)ms vs (105.18 ± 15.94)ms, LV(162.62 ± 7.04)ms vs (110.45 ± 6.92)ms, RV(152.21 ± 30.49)ms vs (131.06 ± 12.04)ms] were significantly prolonged, FAPD dispersion (FAPDd) significantly increased [thoracic spinal cord 1-5(13.3 ± 9.11)ms vs (9.36 ± 7.01)ms] in stress group compared with the control group. Disarrangement of myocardial cells, proliferation of collagen fiber, infiltration of neutrophil and lymphocytes in the cardiac tissue were also observed and distribution of GAP-43, TH and CHAT was significantly increased in stress group. (2) All these changes could be partly reversed by the treatment with fluoxetine.</p><p><b>CONCLUSION</b>Metal stress induced cardiac autonomic nerve and myocardial electrophysiological remodeling and ventricular arrhythmia in rats which could be significantly attenuated by fluoxetine in this model.</p>