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[Abstract ] Objective Modern pharmacological studies confirmed Zhigancao Decoction total extract, single active ingredients and their combinations could obviously inhibit arrhythmia.This study was to investigate the effects of Zhigancao Decoction medicated serum combined with myocardial tissue/silicon substrate microelectrode arrays (MEA) on rapid atrial pacing(RAP). Methods New Zealand white rabbits were randomly divided into normal control group, normal serum control group, Zhigancao Decoction medica-ted serum group and water decoction group, 8 in each group.After the establishment of an atrial fibrillation rabbit model, the field ac-tion potential duration ( fAPD) of the right atrial appendage ( RAA ) tissue was measured and the effections of Zhigancao Decoction medicated serum and water decoction on the fAPD of RAA were observed. Results The successful modeling of rapid atrial pacing induced atrial fibrillation in rabbits contributed to the significant shortening of fAPD 12 h after pacing compared to that before pacing ([174.30 ±1.36]ms vs[162.48 ±0.88]ms, P<0.05).After giving 10%~25% Zhigancao Decoction medicated serum and water decoction, the fAPDs of RAA tissue in rabbits with atrial fibrillation were prolonged, which represented positive dose-response relation-ship.The fAPDs of the rabbits given serum containing 10%, 15%, 20%and 25%Zhigancao Decoction were respectively (170.81 ± 0.61)ms, (171.00 ±0.46)ms, (179.08 ±0.67)ms, (179.76 ±2.26)ms, which were longer than those of water decoction group ([163.82 ±0.780]ms, [163.66 ±0.95]ms, [174.06 ±1.32]ms, [176.84 ±1.19]ms), and the difference was statistically sig-nificant (P<0.05). Conclusion The fAPD can be taken as one index of cardiac electrophysiological change, and 10%~25%Zh-igancao Decoction medicated serum can lead to fAPD extension in rabbit model of atrial fibrillation, which might be the electrophysio-logical mechanism of anti-atrial fibrillation.
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Objective In this research we established rapid atrial pacing rabbit models, to investigate the effects of simvastatin on changes of early atrial effective refractory period (AERP) and protein expression of atrial α1c sub-unit of L-type calcium channel on atrial remodeling. Methods 42 rabbits were randomly divided into 3 groups:control group,rapid pacing group and simvastatin group,simvastatin 5 mg/( kg·d) was given intragastrically daily for two weeks before electrophysiology study in simvastatin group, normal saline was given intragastrically in control and rapid pacing group instead. Control group with no pacing, in simvastatin group and rapid pacing group, right atrium was paced at 800 beats/min for 8 hours to establish acute atrial fibrillation models, right atrial effective re-fractory period(AERP)was measured at the basic cycle length of 200 ms and 150 ms before pacing and 1,2,4,6, and 8 hours after the onset of the pacing, the changes of rate adaptation of AERP (AERP200-AERP150) were ana-lyzed . Right atrium tissue was obtained for measurement of protein expression of atrialα1 c subunit of L-type calcium channel by Western blot. Simultaneously,lipid levels in each group was examined. Results No significant differ-ence in lipid levels among three groups was observed. The AERP was shortened and the rate adaptation of AERP (AERP200-AERP150) disappeared during pacing compared with those before pacing(P<0.05). The shortening of AERP was reversed and AERP200-AERP150 was maintained in simvastatin group. Compared with the control group,the protein expression levels of atrial α1c subunit of L-type calcium channel decreased significantly after 8 hours pacing in rapid pacing group(P<0.01). The protein expression levels of simvastatin group decreased insig-nificantly . Conclusion Atrial rapid pacing can induce the shortening of the AERP and the losing of adaptability to the frequency of AERP,pretreatment with simvastatin can improve the degree significantly and maintain the adapta-bility to frequence basically. The protein expression levels of atrial α1c subunit of L-type calcium channel de-creased significantly after 8 hours pacing,pretreatment with simvastatin can prevent this change without lowering the lipid levels,thus contributing to the ionic mechanism of simvastatin for antiarrhythmia.
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Aim To determine the effects of sodium tashinoneⅡA sulfonate(TSN) on monophasic action potential(MAP) and tachycardia-induced electrical remodeling of rabbit atria in vivo.Methods Twenty-four rabbits were equally divided into two groups randomly: control group and TSN group.Electrical catheters were localized in the right atrium through right internal jugular vein.Right atrial MAP was recorded by multiple channel recording. ERP of right atrial(AERP) was assessed by programmed electrical stimulation before pacing and from 0～8 hours after the onset of the pacing.Results The AERP_(200 ms) of control group was shortened from (105.9?3.8) ms to(114.7?7.2) ms and the rate-dependent of control group's atrium was lost through the pacing process compared with TSN group before pacing(P
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Obiective To investigate the influence of rapid atrial pacing(RAP)on the expression of ?1c subunit of L-type calcium channel,and the protective effect of verapamil.Methods 30 rabbits were randomly assigned into RAP group and verapamil pre-conditioned group.Each group was further divided into 5 subgroups(n=3 for each subgroup).Electrode was embedded in the right atrium through right external jugular vein.Pacing was performed for 6h,12h,24h and 48h in different subgroups.No pacing in the sham operation group.For verapamil pre-conditioned group,the drug was intravenously administered(0.2mg/kg)30 minutes before the initiation of rapid atrial pacing.Right atrium tissue was harvested for determination of mRNA and protein expression of L-type calcium channel subunits by reverse transcription polymerase chain reaction(RT-PCR)and Western blot.Results The mRNA level of ?1c subunit started to be reduced 6h after rapid atrial pacing(RAP)and continued to decline as pacing continued,and the expression of protein was parallel with mRNA.Otherwise,the mRNA level of ?1c subunit started to decrease 24h after RAP and continued to decline while pacing continued,and the expression of protein paralleled with that of mRNA in verapamil pre-conditioned group.Verapamil can attenuate the down-regulation of L-type calcium channel of the atrium induced by RAP only at 24h after RAP,but the effect was less intent.Conclusion mRNA and protein expression level of L-type calcium channel subunits decreased after RAP,The calcium channel blocker verapamil can attenuate the down-regulation of L-type calcium channel of atrium induced by RAP resulting in a decrease or postponement of calcium overload in atrial myocytes,thus exerting protective effects on atrial electrical remodeling,but such effects vanished after prolonged pacing.
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AIM: To investigate the potassium channel gene expression of myocardial sleeves of pulmonary vein and effects of amiodarone on rabbits with rapid atrial pacing.METHODS: Rabbits were divided into three groups(n=10),(1) the control group with sham operation and placebo;(2) the right atrial pacing(RAP) group at 600 beats/min with the placebo;(3) the amiodarone group treated for seven days with oral amiodarone at 100 mg ? kg-1 ? d-1.Based on RAP simultaneously,the messenger ribonucleic acid(mRNA) of specimen was measured by reverse transcription-polymerase chain reaction.RESULTS: Compared with the control group,Kv4.3(transient outward K+ current,Ito1) mRNA expression in RAP group was reduced by 51%(P
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BACKGROUND: Pacing-induced atrial electrical remodeling (AER) is characterized by shortening of atrial effective refractory period (A-ERP) and its altered rate adaptation. In paroxysmal atrial fibrillation (AF), periods of AF occur with interveneing normal sinus rhythm (NSR) when atria recover from the preceding AER. Previous episodes of AF may precondition the atrial myocardium and cause different time course of AER in subsequent episodes of AF. But the influence of the preceding AER on the subsequent AER has not been described. METHODS: Four mongrel dogs were anesthetized with enflurane. After thoracotomy, silicon band with 3 pairs of electrodes was sutured to the lateral wall of the left atrium. Atrial pacing was performed after 2 wks of recovery and autonomic blockade. Pacing protocol consisted of rapid atrial pacing (RAP) at 500 bpm (for 60 min) and recovery in NSR (for 60 min) which was repeated three times. A-ERP was measured every 10 min. The same pacing protocol was repeated after pretreatment with verapamil (0.1 mg/kg/hr). RESULTS: 1) With 60 min of RAP, A-ERP decreased significantly (126+/-6 ms vs. 105+/-7 ms, p<0.005). 2) After cessation of pacing, A-ERP returned to 98% of baseline value in 15 minutes. Recovery from AER occurred faster than AER (78 vs 21 ms/h). 3) After pretreatment with verapamil, RAP decreased A-ERP from 127+/-5 ms to 116+/-5 ms. AER, the reduction in A-ERP, was significantly attenuated by pretreatment with verapamil (deltaERp=17+/-7 vs. 9+/-0.2 %, p<0.05). 4) When RAPs were repeated, AER showed a tendency of acceleration, but it was not statistically significant (deltaERp=22 ms, 24 ms, 28 ms at the end of 60 min pacing for the 1st, 2nd, 3rd pacing). CONCLUSION: RAP induced AER in conscious dog atria and it was reduced by pretreatment with calcium channel blocking agent, verapamil. Upon repeated atrial stimulations, AER did not accelerate or decelerate when the atria recovered from the preceding AER.