| Background The pathogenesis of atrial fibrillation (AF) is indefinite. The mostadmissive hypothesis is that it correlates with the rapid electrical activity in pulmonaryveins (PV) and the microreentry in left atrium. Recently, studies certified that therewere complex relationship among AF, oxidative stress and autonomic nervous system(ANS). Oxidative stress correlates with interstitial fibrosis of atrium, and interstitialfibrosis plays an important role in structural reconstruction of atrium, which is one ofthe pathogenesis of AF. ANS also plays an important role in AF’s initiation andmaintenance, which is characterized by atrial electrical remodeling (AER). Meanwhile,there is a synergetic effect between oxidative stress and ANS in AF’s initiation andmaintenance. The aim of this study is to explore the effect of vagosympathetic trunksstimulation on oxidative stress in dogs with rapid atrial pacing (RAP).Methods: Twenty four mongrel dogs were randomly divided into four groups:cervical vagosympathetic nerve stimulation (VNS) group, RAP group, VNS+RAPgroup and autonomic blockade+RAP group. Bilateral cervical vagosympathetic trunkswas isolated in every dog, and the cranial ends of the vagosympathetic nerves wereligated. A pair of teflon-coated silver wires was inserted into the cervicalvagosympathetic trunks for stimulation. A bipolar pacing catheter was inserted in theright atrium by the way of the right femoral vein. In VNS group, vagosympathetic nervewas suffering electric stimulation by the silver wires connected with vagus stimulator inorder to decrease the baseline heart rate by50%. In RAP group, The rapid atrial pacingat600beats/min with a square waves of2×threshold and1ms duration induced a acuteAER. In VNS+RAP group, dogs underwent both VNS and RAP. In autonomic blockade +RAP group, dogs were injected metoprolol and atropine parenteral solution, thenreceived rapid atrial pacing. Blood samples were collected at0h,1h,2h,3h,4h,5h,6hafter above operation. Enzyme linked immunosorbent assay (ELISA) was preformed tomeasure the level of serum Reactive Super Oxide Dismutase (SOD), Oxygen Species(ROS) and Glutathione Peroxidase (GSH-Px).Results: In VNS group, Baseline SOD level was73.34±3.41U/ml, the SOD levelat1h,2h,3h,4h,5h and6h during stimulation were74.19±3.11U/ml、75.21±3.56U/ml、76.51±3.50U/ml、78.32±3.68U/ml、78.06±3.79U/ml、76.45±3.67U/ml.Baseline ROS level was166.47±12.27U/ml, the ROS level at1h,2h,3h,4h,5h and6h during stimulation were165.79±16.66U/ml、158.71±15.35U/ml、153.65±13.58U/ml、147.91±10.53U/ml、150.61±12.91U/ml、157.26±14.32U/ml. BaselineGSH-Px level was55.14±2.68U/L, the GSH-Px level at1h,2h,3h,4h,5h and6hduring stimulation were56.20±2.64U/L、57.14±2.72U/L、58.13±2.93U/L、59.57±3.03U/L、58.85±2.98U/L、58.35±2.93U/L. With VNS, there were no significantdifferences in the serum levels of SOD, ROS, GSH-Px throughout the6-hourstimulation period (P＞0.05). At RAP group, Baseline SOD level was73.34±1.01U/ml,the SOD level at1h,2h,3h,4h,5h and6h during RAP were78.63±1.26U/ml、86.86±2.24U/ml、96.85±3.27U/ml、106.71±2.43U/ml、115.38±2.62U/ml、122.32±2.45U/ml. Baseline ROS level was167.08±4.66U/ml, the ROS level at1h,2h,3h,4h,5h and6h during RAP were186.12±6.22U/ml、218.82±6.93U/ml、246.70±8.94U/ml、283.15±9.29U/ml、309.41±5.82U/ml、344.00±8.57U/ml. Baseline GSH-Pxlevel was53.09±1.15U/L, the GSH-Px level at1h,2h,3h,4h,5h and6h during RAPwere58.83±1.86U/L、68.41±1.83U/L、78.15±2.37U/L、88.39±2.66U/L、97.05±2.08U/L、107.21±2.55U/L. The SOD, ROS, GSH-Px levels elevated markedly afterRAP, and were progressively elevated throughout the6-hour pacing period (P＜0.05).In VNS+RAP group, Baseline SOD level was72.56±1.86U/ml, the SOD level at1h,2h,3h,4h,5h and6h during stimulation were80.42±3.78U/ml、95.18±4.79U/ml、107.40±3.96U/ml、117.73±4.25U/ml、128.47±3.36U/ml、136.57±2.98U/ml.Baseline ROS level was169.95±4.82U/ml, the ROS level at1h,2h,3h,4h,5h and6hduring stimulation were210.15±7.93U/ml、255.18±5.65U/ml、295.92±5.62U/ml、323.25±7.41U/ml、350.06±9.67U/ml、370.30±11.30U/ml. Baseline GSH-Px levelwas53.63±1.24U/L, the GSH-Px level at1h,2h,3h,4h,5h and6h during stimulationwere64.71±1.87U/L、77.45±2.12U/L、90.10±3.30U/L、99.11±2.94U/L、108.04±2.79U/L、114.96±2.59U/L. The SOD, ROS and GSH-Px levels elevated markedly after RAP, and were progressively elevated throughout the6-hour pacing period.Compare with RAP Group, SOD, ROS and GSH-Px levels are higher in each hour afterRAP in VNS+RAP group throughout the6-hour pacing period (P＜0.05). In autonomicblockade+RAP group group, Baseline SOD level was70.84±1.40U/ml, the SOD levelat1h,2h,3h,4h,5h and6h during stimulation were73.98±1.15U/ml、78.62±2.03U/ml、83.65±2.94U/ml、88.57±2.90U/ml、94.49±2.80U/ml、98.82±2.76U/ml.Baseline ROS level was166.07±4.48U/ml, the ROS level at1h,2h,3h,4h,5h and6hduring stimulation were174.91±3.47U/ml、184.83±3.49U/ml、195.28±4.77U/ml、206.81±7.22U/ml、218.87±7.52U/ml、230.66±8.45U/ml. Baseline GSH-Px levelwas52.53±1.40U/L, the GSH-Px level at1h,2h,3h,4h,5h and6h during stimulationwere55.34±1.35U/L、58.64±1.02U/L、61.69±1.59U/L、65.00±2.29U/L、69.13±2.19U/L、72.10±2.27U/L. The SOD, ROS and GSH-Px levels elevated markedlyafter RAP, and were progressively elevated throughout the6-hour pacing period.Compare with RAP Group, SOD, ROS and GSH-Px levels are lower in each hour afterRAP in VNS+RAP group throughout the6-hour pacing period (P＜0.05).Conclusions: RAP could result in oxidative stress. Further, VNS without RAPcouldn’t cause oxidative stress, but VNS could aggravate the oxidative stress caused byRAP. These findings suggested that ANS with RAP could result in electricalremodeling via oxidative stress. |
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