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To observe the effects of hypothermia on the repolarization duration and the expression of Kir2.1 protein of ventricular myocytes in isolated rat heart and explore the role of Kir2.1 protein. Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups (n=6 per group): Control group (C group), 35℃ group (H group), 32℃ group (H group). Langendorff isolated heart models were established. After 15 min 37℃ K-H fluid banlanced perfusion, C group continued to perfuse the K-H solution at 37℃ for 30 minutes, H group continued to perfuse the K-H solution at 35℃ for 30 minutes, H group continued to perfuse the K-H solution at 32℃ for 30 minutes. At 15 min of balanced perfusion (T), and 30 min of continuous perfusion (T), the heart rate,and the MAP in the three layers of the left ventricular anterior wall were recorded, the action potential duration at 50% repolarization (MAPD), the action potential duration at 90% repolarization (MAPD) and transmural dispersion of repolarization(TDR) were calculated. At the same time, the occurrence of arrhythmia was recorded. The expression of Kir2.1 protein was measured by Western blot. The average optical density (AOD) and the distribution of Kir2.1 protein were measured by immunohistochemistry in the ventricular tissue measured by electrophysiology. Compared with T, the heart rate was decreased, MAPD and MAPD were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) in H group, H group at T. Compared with C group, the HR was decreased, the MAPD was prolonged significantly (P＜0.05), TDR was increased significantly (P＜0.05),the expression and the AOD of Kir2.1 protein were decreased significantly (P＜0.05) in Hgroup, Hgroup at T. Compared with H group, the heart rate of H group was decreased significantly (P＜0.05), MAPD and MAPD were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) at T. The distribution of Kir2.1 protein in group C was normal, while the distribution of Kir2.1 in H group and H group was disordered. Hypothermia prolonged the ventricular duration of repolarization and increased the dispersion of repolarization. The mechanism is related to the down-regulation the expression of Kir2.1 protein and the disorder of the distribution of Kir2.1 protein.
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Objective To investigate the electrophysiological protective effect of HTK solution containing sevoflurane on rat cardiac transplantation. Methods Twenty-four male Sprague-Dawley rats were divided into the control group,sevoflurane group and Heptanol group. Rat hearts in 3 groups were stored in HTK solution,containing sevoflurane and sevoflurane+heptanol HTK solution for 6 h. Heart resuscitation time,the duration of arrhythmia and monophasic action potential(MAP)and heart rate(HR)at different time points were recorded.Monophasic action potential duration of repolarization at 50% and 90%(MAPD50 and MAPD90),monophasic action potential amplitude(MAPA)and maximal velocity(Vmax)were analyzed. Results The isolated rat hearts in each group can be successfully restored to the spontaneous heart beat. Compared with group C ,heart resuscitation time in group S and group H was significantly shortened,heart rate(HR)was significantly decreased at T1,MAPD50 and MAPD90 in heart intima and epicardium were shortened at T1 ~ T2,the incidence of ventricular fibrillation and reperfusion arrhythmia Scores were reduced,with the shorter duration of ventricular fibrillation(P<0.05). No significant difference was found in Vmax and MAPA among the three groups at each time point. Conclusion HTK solution containing sevoflurane and HTK solution containing heptanol had similar electrophysiological effects ,which could inhibit the prolonged monophasic action potential(MAP)and reduce arrhythmia. The electrophysiological protective effect of HTK solution containing sevoflurane may be associated with the inhibition of gap junction function.
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Objective To study the effects of different concentrations of sevoflurane on monophasic action potentials (MAPs)of three-layer myocardium of ischemia reperfusion in isolated rat hearts.Methods Thirty-two healthy SD male rats,weighing 280-320 g,were randomly divided into four groups after successful preparation of langendorff isolated heart perfusion model and 1 5 min perfusion and balance of K-H fluid.In the ischemia-reperfusion group(group IR),K-H fluid perfusion was stopped and balanced for 15 min and cardiac arrest was induced for 60 min with the injection of Thomas solution (4℃,20 ml/kg)while the heart was protected by the low temperature Thomas so-lution (4℃)around it.Reperfusion of Thomas solution (4℃,10 ml/kg)was performed for 30 min and the heart was resuscitated by the perfusion of K-H fluid for 60 min.In the 0.5 MAC sevoflurane group (group Sev0.5 ),K-H fluid contained 0.5 MAC sevoflurane and other procedures were the same as in group IR.1.0 MAC sevoflurane group (group Sev1.0 ),K-H fluid contained 1.0 MAC sevoflurane and other procedures were the same as in group IR.2.0 MAC sevoflurane group (group Sev2.0),K-H fluid contained 2.0 MAC sevoflurane and other procedures were same as in group IR. HR,MAPs including time course (MAPD50,MAPD90)and MAP amplitude of endocardium,mid-layer myodardium and epicardium was recorded at the time of continuous balance perfusion for 1 5 min (T0),continuous perfusion for 15 min (T1),reperfusion for 15 min (T2)and 30 min (T3). Results Compared with T0and T1,HR was slower at T2and T3(P<0.05);Compared with group IR at T2and T3,HR in group Sev0.5 and group Sev1.0 was higher,that in group Sev2.0 was slower P<0.05);At T2,arrhythmia was observed in 6 rats in group IR,while arrhythmia was observed in 1 rats in group Sev0.5 ,and arrhythmia was observed in 2 rats in group Sev1.0 and arrhythmia was observed in 1 rats in group Sev2.0;Compared with group IR at T3,MAPD50in group Sev0.5 was shorter in three sites(P<0.05);Compared with group IR at T3,MAPD90in other three groups was shorter.Conclusion Different concentrations of sevoflurane can shorten MAPD90of MAPs,and the effects don＇t depend on the concertrations of sevoflurane when it changes from 0.5 MAC to 2.0 MAC;which may be the mechanism of decreased arrhythmias risk caused by sevoflurane.
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Objective To observe the effects of granulocyte colony stimulating factor (G-CSF) on electrophysiological properties of post-infarct ventricles.Methods Sixty-seven survival Wistar rats were divided into 4 groups:Sham group,Control group,MI early G-CSF group (E-G) and MI delay G-CSF group (D-G) after ligation of the left coronary artery as myocardial infarction model.Monophasic action potential(MAP) was recorded by absorption electrode in ex vivo perfused rat hearts.Effective refractive period(ERP),sinus cardiac length (SCL),action potential amplitude (APA),maximal depolariged (Vmax),ventricular fibrillation threshold(VFF) and ventricular fibrillation duration(VFD) were measured.Results The electrophysiological parameters (SCL,VFT,VFD,APA,ERP/MAP90,dispersion of ERP and MAP90) of the E-G group were improved significantly (all P ＜ 0.05) at day 7 post MI.Improvement in SCL,dispersion of ERP and MAP 90 were found in the D-G group as well at day 7 post MI (all P ＜ 0.05).Substained improvement in electrophysiological parameters were found in the E-G group at 3 months after MI (P ＜0.05).Besides SCL,APA,Vmax and dispersion of MAP90,all other parameters in the D-G group were similar to that of the control group with no statistical significance and even had a tendency of deterioration in ERP and MAP90 3 months after MI.Conclusion G-CSF intervention could improve electrophysiological properties of ischemic ventricles.Early G-CSF intervention showed better outcomes compared to delay G-CSF intervention on electrical remodeling ischemia myocardiumwhich may have effect on reducing the development of ventricular arrhythmia.
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Objective To study the effects of dexmedetomidine on the monophasic action po-tential duration and the transmural dispersion of repolarization during ischemia-reperfusion of isolated rabbit hearts and thus explore its effect on myocardial ischemia-reperfusion electrophysiological char-acteristics.Methods Eighteen healthy adult rabbits,weighing (2.0±0.5)kg,were randomly divided into 3 groups after successful preparation of Langendorff isolated heart perfusion model and 1 5 min perfusion and balance of K-H fluid.In the control group (group C),37 ℃ K-H fluid was continuously perfused and balanced for 1 50 min.In the ischemia/reperfusion group (group IR),K-H fluid was stopped after continuous perfusion and balance for 1 5 min and cardiac arrest was induced for 60 min with the injection of Thomas solution (4 ℃,10 ml/kg)while the heart was protected by the low tem-perature Thomas solution (4 ℃)around it.Reperfusion of Thomas solution (4 ℃,5 ml/kg)was performed for 30 min and the heart was resuscitated by the perfusion of K-H fluid for 60 min.In dexmedetomidine group (group DEX),dexmedetomidine (25 ng/ml)was added in the K-H fluid and the Thomas solution.Other procedures were same as in group IR.Heart rate(HR),monophasic ac-tion potential amplitude (MAPA)of the three layers of heart [endocardium (Endo),myocardium (Mid)and epicardium (Epi)],0 phase maximal increase rate (Vmax),90% monophasic action po-tential duration (MAPD90 )and transmural dispersion of repolarization (TDR)were recorded at the time of continuous balance perfusion 1 5 min(T0 ),continuous perfusion 1 5 min/balance 30 min(T1 ), reperfusion 30 min/balance 120 min(T2 )and reperfusion 60 min/balance 1 50 min(T3 ).Cardiac ar-rhythmia and resuscitation time at cardiac reperfusion were observed,without using drugs to restore normal cardiac rhythm.Results In group DEX,cardiac resuscitation time was significantly shorter (1 6.67±3.78)s than that in group IR (46.33±7.29)s (P <0.05);At T2 ,in group IR,arrhythmia was seen in 6 rabbits and normal cardiac rhythm was restored within 2 min in two rabbits,while in group DEX,arrhythmia was seen in 2 rabbits and normal cardiac rhythm was restored within 2 min in one rabbit,without the use of any drugs.When compared with T0 ,HR was slower at T2 and T3 in group IR and at T1-T3 in group DEX (P <0.05);Compared with T1 ,HR was slower at T2 and T3 in group DEX (P <0.05);Compared with T2 and group C,HR was slower at T3 in group DEX;At T1-T3 ,HR in group DEX were significantly slower than that in group IR (P <0.05).Compared with T0 ,MAPD90 of Mid at T1 and Epi,Mid,Endo at T2 and T3 in group DEX were significantly extend-ed (P <0.05);Compared with T1 ,MAPD90 of Epi,Mid,Endo in group DEX were significantly ex-tended at T3 ;MAPD90 of Mid in group DEX was significantly longer than that in group C at T3 (P <0.05);At T2 and T3 ,MAPD90 of Epi,Mid,Endo in group DEX were longer than that in group IR (P <0.05).Compared with T0 and group C,TDR at T2 and T3 in group IR and at T1-T3 in group DEX significantly increased (P <0.05),while TDR in group DEX were less than that in group IR at T2 and T3 (P <0.05).Conclusion Dexmedetomidine appeared to prolong MAPD and restrain the dis-proportion of resuscitation of myocardial ischemia-reperfusion injury.Dexmedetomidine could have the effect of stabilizing myocardial ischemia-reperfusion electrophysiological characteristics.
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Objective: To explore the relationship between expression of tumor necrosis factor-α( TNF-α) and electrophysiological heterogeneity in isolated heart tissues and isolated rat ventricular myocytes.The arrhythmogenic mechanisms of TNF-αwere further studied.Methods:Langendorff perfused heart tissues models were used to verify the arrhythmogenic effects of TNF-α.The monophasic action potentials( MAPs) of the endocardium and epicardium from the isolated heart tissues were recorded by elec-trophysiological experiments.The isolated rat ventricular myocytes were obtained by enzymatic dissociation.K+currents(Ito,IK1)were recorded by using whole cell patch clamp technique.Results: Compared to the control group, the difference in MAPD between endocardium and epicardium dramatically increased with TNF-α( P<0.05 ) .TNF-αcould cause MAP duration ( MAPD ) prolongation, and a single dose of TNF-αdifferentially affected the MAPs of endocardium and epicardium of isolated heart tissues.Compared to the control group,the K+currents(Ito,IK1)were dose-dependently decreased with TNF-αin rat ventricular myocytes(P<0.05).However, etanercept had no effects on the MAPD in the absence of TNF-α.Conclusion:TNF-α-induced heterogeneity of MAPD between the endo-cardium and epicardium may provide the substrate for the onset of ventricular arrhythmias during acute myocardial infarction.The effect might be associated with TNF-αcontribute to re-entrant ventricular arrhythmias which resulted from decreased K+currents(Ito,IK1).
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AIM:To study the effect of remifentanil on monophasic action potential and transmural dispersion of repolarization (TDR) in the 3-layer myocardium of isolated rabbit hearts .METHODS:Adult rabbits (n=18, 2.0 ~2.5 kg) were used to isolate the hearts for preparing Langendorff perfusion model .The hearts were randomly divided into 3 groups after perfusion with K-H solution for 15 min: the perfusion in control group ( C group ) continued for 60 min; the hearts in remifentanil group ( R group ) were perfused with 12 μg/L remifentanil K-H solution for 60 min; the hearts in remifentanil+aminophylline group ( RA group ) were given 60-min perfusion of 12 μg/L K-H remifentanil +30 mg/L aminophylline .The HR and 3 layers of myocardial monophasic action potential ( MAP) in the left ventricular anterior wall were recorded at time points after balanced infusion for 15 min ( T0 ) , and continued perfusion for 15 min ( T1 ) , 30 min ( T2 ) and 60 min ( T3 ) .The monophasic action potential duration of repolarization at 90%( MAPD90 ) and the transmural dispersion of repolarization (TDR) were calculated.The early afterdepolarization, delay afterdepolarization and arrhythmia were also observed.RESULTS:In R group, slower HR and prolonger MAPD90 and TDR at T1 ~T3 were observed as com-pared with those at T0(P<0.05).R group showed slower HR and longer MAPD 90 and TDR than C group and RA group (P<0.05).CONCLUSION:Remifentanil slows the HR, extends the MAPD90 and increases the TDR, thus being prone to induce reentry.Aminophylline makes HR faster and MAPD90 shorter, thereby reducing the TDR.
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Objective To investigate the effect of positive acceleration (+Gz) on monophasic action potential duration of 90%repolarization( MAPD90 ) and transmural dispersion of repolarization ( TDR) in ventricles of rabbits and to explore the cellular electrophysiologic mechanism of tachyarrhythmia induced by positive acceleration .Methods Twenty-four healthy, male New Zealand white rabbits were randomly and equally divided into control group and +Gz group.The +Gz group rabbits were given +8 Gz exposure, 1 min a time, 3 times a day,and a total of 7 days.The two groups were subjec-ted to Holter monitoring at the same time to observe the incidence of tachyarrhythmia .Using the monophasic action potential ( MAP) recording technology , the MAP of the left ventricle was recorded while MAPD 90 and TDR were measured .By using Burst stimulation method , the right ventricular anterior wall of the rabbits was stimulated , and the incidence of tachya-rrhythmia was observed .Results The Holter record showed that the incidence of tachyarrhythmias in +Gz group was 55%(6/11), but the control group did not have any case of tachyarrhythmias .Compared with the control group ,MAPD90 of en-docardial and epicardial cells was significantly decreased in the +Gz group, while MAPD90 of middle myocardial cells did not change significantly ,but TDR was increased obviously .Four rabbits in +Gz group suffered from tachyarrhythmias dur-ing Burst stimulation ,and the incidence of tachyarrhythmias was 40% ( 4/10 ) .Conclusion +Gz exposure can increase the incidence of tachyarrhythmias .The shortened MAPD90 of ventricular muscle cells and the increased TDR may be the cell electrophysiological mechanisms of tachyarrhythmias induced by +Gz.
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BACKGROUND:Ventricular arrhythmia (VA) is one of the most common complications of myocardial infarction (MI), and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits. METHODS:Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups:sham-operated (SHAM) group (n=8), MI group (n=8) and MI with ramipril (RAM) group (n=8). Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and III. After MI, rabbits in the RAM group were fed with intragastric ramipril (1 mg/kg per day ) for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation (VT/VF) episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student'st test and ANOVA were used for statistical analysis. RESULTS:VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks (2.6±0.8 vs. 12.4±2.9,P<0.05). Twelve weeks after MI, the duration of repolarization for 90％ (APD90) of three-tier ventricular myocytes in the MI group was longer than that before MI (258.2±21.1 vs. 230.1±23.2, 278.0±23.8 vs. 245.8±25.4, 242.6±22.7 vs. 227.0±21.7,P<0.05). However, the APD90 was not significantly different at 12 weeks before and after MI in the RAM group (P>0.05). Moreover, the transmural dispersion of repolarization (TDR) was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups (36.2±10.2 vs. 18.7±6.2, 24.9±8.7,P<0.05). But the TDR was not significantly different between the RAM and SHAM groups (18.7±6.2 vs. 24.9±8.7,P>0.05). CONCLUSION:Ramipril may reduce the incidence of malignant ventricular arrhythmia via improvement of transmembrance repolarization heterogeneity after MI.
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Objective To determine whether specific angiotensin-conventing enzyme inhibitor with ramipril would affect ventricular arrhythmia generation in rabbits after myocardial infarction and discuss the mechanism of its antiarrhymic efficacy.MethodsTwenty-four New Zealand rabbits (Wuhan Laboratory Animal Research Center) were separated into 3 groups:sham-operated (SHAM) group (n =8 ),myocardial infraction (MI) group ( n =8) and myocardial infraction with ramipril (RAM) group ( n =8).SHAM group received a median sternotomy without left ventricular coronary artery ligation.MI and RAM groups' rabbits received a median sternotomy followed by left coronary artery ligation. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead Ⅱ and Ⅲ.After MI,RAM group rabbits were fed with ramipril [ 1mg/ ( kg · d) ]by intragastric administration for 12 weeks.Before and after MI 12 weeks in three groups.Ventricular tachycardia or fibrillation episodes and the monophasic actionpotential duration in epicardium,mid-myocardium and endocardium cadiocytes were recorded.The statistical technique was t-test and ANOVA.Results Ventricular tachycardia or fibrillation episodes were markedly decreased in RAM group than that in MI group after 12 weeks [ (2.6 ± 0.8) vs.(12.4 ± 2.9),P ＜0.05 ].After MI 12 weeks,the action potential duration of repolarization 90％ (APD90) of three-tier ventricular myocytes in MI group was prolonged than that before MI [ (258.2 ±21.1 ) vs.(230.1 ±23.2),( 278.0±23.8 ) vs.(245.8±25.4),(242.6±22.7) vs.(227.0±21.7),P＜0.05]; however,it was not significant difference between before and after MI 12w in RAM group (P ＞ 0.05 ).Moreover,the transmural dispersion of repolarization(TDR) was markedly increased after MI 12w in MI group than in SHAM and RAM group [ (36.2 ± 10.2 ) vs.( 18.7 ± 6.2 ),(24.9 ± 8.7 ),P ＜ 0.05 ]; but the TDR was not significant difference between RAM and SHAM group ( 18.7 ± 6.2 ) vs.( 24.9 ± 8.7 ),P ＞ 0.05].ConclusionsRamipril significantly reduced the malignant arrhythmia incidence in rabbits after MI.Mended the abnormal TDR was the mechanism for ramipril to therapy.
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Objective To study the effect of berberine on arrhythmia caused by stretch of rats' myocardium,in vitro,after myocardial ischemia (MI) for 30 min.Methods The study was carried out in the laboratory of Heilongjiang traditional Chinese medicine university.A total of 40 Wistar rats were randomly (random number) divided into 4 groups,namely normal control group,berberine group、MI group and MI + berberine group.After perfusion of rat' s heart with Langendorff perfusion device,the model of MI was made with ligation of left anterior descending branch for 30 min.Berberine was dissolved in Tyrode' s solution to a concentration of 300 μmol/L.The hearts were stretched for 5 s by 0.2 ml.The effect of stretching was observed for 30 s to record 90％ monophasic action potential (MAPD90),premature ventricular beats (PVB) and ventricular tachycardia (VT).Quantitative data were compared with ANOVA.Qualitative data were compared with a x2 test.Differences with a value of P ＜ 0.05 were considered statistically significant.Results MAPD90 in normal control and MI group obviously prolonged after the hearts were stretched ( P ＜ 0.01 ).And MAPD90 in MI group was even longer than that of normal control group (P＜0.05).Berberine had no influence on MAPD90 before myocardiuml stretched (P ＞0.05),while it could reduce the degree of prolongation in MAPD90 after myocardium stretched (P ＜ 0.05 or P ＜0.01 ).The incidence rate of PVB and VT in normal control and MI group increased after stretched.The berberine in dose of 300 μmol/L could reduce the incidence of PVB and obviously inhibit the occurrence of VT ( P ＜ 0.01 ).Conclusions Berberine could obviously inhibit the occurrence of stretch-inducedarrhythmias after myocardial infarction.
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@#ObjectiveTo investigate the effect of hyperlipidemia on monophasic action potential and calcium current of heart in rabbits.Methods24 rabbits were divided into the high cholesterol group (n=12) and control group (n=12) and fed with high cholesterol forage and standard forage respectively for 10 weeks. Electrocardiograph, ventricular fibrillation threshold and the level of serum lipid were examined. Whole-cell patch clamp technique was used to record I_ Ca-L.ResultsIn high cholesterol group, the serum cholesterol level was higher than the control group ( P<0.01), ventricular fibrillation threshold (10.2±1.7 V) lower than that of the control group (13.9±1.3 V)( P<0.05), MAPD90 displayed more significant rate-dependent prolongation. At cycle lengths of 1500 ms, MAPD90 was 358±18 ms in the high cholesterol group, while it was 277±20 ms in the control group. The densities of ICa-L were larger in the high cholesterol group (14.7±0.8 pA/pF) than that in the control group (10.9±1.1 pA/pF)( P<0.01).ConclusionHypercholesterolemia can produce cardiac electrical remodeling, including increased ICa-L, prolonged repolarization and decreased ventricular fibrillation thresholds.
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The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly: acute ischemia (AI) group and sham operation (SO) group. By using the monophasic action potential (MAP) technique, MAP and effective refractory period (ERP) of thethree layers myocar dium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization (TDR) and transmural dispersion of ERP (TDE) were analyzed. The results showed that in the AI group, MAP duration (MAPD) was shortened from 201.67±21.42 ms to 169.50±13.81 ms (P＜0.05), but ERP prolonged to varying degrees and TDE increased during ischemia.In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.
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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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BACKGROUND: This study was designed to evaluate the role of KATP channel activation and change of monophasic action potential duration on cardioprotective effect of ischemic preconditioning in cat. METHODS: 34 cats were divided into 4 groups: control (n=10), ischemic preconditioning(n=8), glibenclamide pre-treated(n=8) and nicorandil pre-treated group(n=8). Ischemic preconditioning was done in ischemic preconditioning and glibenclamide pre-treated groups by 3 episodes of 5 min ischemia and 10 min reperfusion. All subjects underwent 40 min of ischemia and 40 min reperfusion. The KATP channel antagonist glibenclamide was given as intravenous bolus (0.5mg/kg) 10 min before ischemic precondtioning and infused (5 microgram/min) during ischemic preconditioning. Nicorandil, a KATP channel opener was injected as intravenous bolus (0.5mg/kg) before 40 min ischemic procedure. Monophasic action potential duration at 50% repolarization(MAP50) was measured in the ischemic and non-ischemic area respectively by epicardial probe throughout the experiment. The effects of ischemic preconditioning were determined by infarct size (% area at risk). RESULTS: Ischemic preconditioning or pretreatment with nicorandil prior to 40 min ischemia demonstrated a significant reduction in infarct size(26.6+/-7%, 33+/-8% infarction of the risk zone, respectively, p<0.01, p<0.05 vs. control) with respect to control(42+/-7% infarction of the risk zone). Pretreatment with glibenclamide abolished the effect of ischemic preconditioning(40+/-8% infarction of the risk zone, p=NS vs. control) Ischemic preconditioning group exhibited a significant reduction of ischemic area MAP50 duration in the ischemic area during preconditioning; at first preconditioning 123+/-9msec vs. 137+/-19msec control(p=NS), at second preconditioning 105+/-16msec vs. 140+/-19msec control(p<0.01), at third preconditioning 109+/-15msec vs. 138+/-19msec control(p<0.05). Pretreatment with glibenclamide prevented the reduction of MAP50 in the ischemic area during ischemic preconditioning. During 40 minutes ischemia, MAP50 shortening was more pronounced in the preconditioned group than in control group; at 10 min 85+/-22 msec vs. 131+/-31msec control(p<0.05), at 20 min 88+/-21msec vs. 130+/-32msec control(p<0.05), and at 30 min 103+/-24msec vs. 136+/-30msec control(p<0.05). This shortening effect was prevented by glibenclamide pretreatment. Nicorandil pretreatment pronounced the ischemic shortening of MAP50 in ischemic area and the nicorandil effect was most significant during early ischemic period; at 10 min 97+/-21msec(p<0.05 vs. control), at 20 min 104+/-32msec (p=NS vs. control), and at 30 min 134+/-28msec(p=NS vs. control). MAP50 measured in non-ischemic area was not significantly different between groups. CONCLUSION: We conclude that KATP channel activation and monophasic action potential duration shortening play a important role in myocardial protection during ischemic injury.
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Animals , Cats , Action Potentials , Glyburide , Infarction , Ischemia , Ischemic Preconditioning , Nicorandil , ReperfusionABSTRACT
BACKGROUND: Monophasic Action Potential(MAP) recording using contact electrode is very sensitive method to detect the ischemic changes of myocardium. The purpose of this study were to investigate changes of MAP during percutaneous transluminal coronary angioplasty(PTCA) and to evaluate through MAP whether or not a brief episode of ischemia influenced on subsequent ischemic episode during PTCA. Method: MAPs using endocardial contact electrode were recorded dbefore, during the fitst and second inflation and 3 min after PTCA in 7 patients undergoing PTCA. RESULTS: 1) MAP amplitude significantly decreased to 79.1+/-11.0% during the first inflation(p<0.05) and to 86.3+/-9.0% during the second inflation(p<0.05) and recovered to 92.7+/-3.7% at 3 min after PTCA. 2) MAP duration to 90% repolarization(MAPD 90) significantly decreased to 91.4+/-5.1% during the first inflation(p<0.05) and to 95.3+/-3.5% dudring second inflation(p<0.05) and recovered to 97.3+/-2.8% at 3 min after PTCA. 3) Double prodducts showed no significant difference between the first and second inflation. 4) The changes of MAP amplitude and MAP duration during the second inflation was significantly lower than that recorded during the first inflation. CONCLUSION: MAP recording using endocardial contact electode may be safe and very sensitive method to detect the ischemic changes of human endocardium and the lessened MAP changes during the second inflation supports the concept of preconditioning ischemia.
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Humans , Action Potentials , Electrodes , Endocardium , Inflation, Economic , Ischemia , MyocardiumABSTRACT
Dauricine ( Dau ) significantly prolonged monophasic action potential duration of 50% and 90% repolarization ( MAPD50 and MAPD90 ) and functional refractory period (FRP)of the hearts in anesthetized cats in dose-dependent manner. At 9 mg/kg of Dau, MAPD50 was increased from 170?19 ms to 197?20 ms; MAPD90 from 216?16 ms to 249?18 ms; FRP from 177 ? 15 ms to 238 ? 20 ms.Dau 5 mg/kg iv followed by constant perfusion for 30 min could prevent the shortening of MAPD50 in the ischemic boundary area ( BA ) and increased FRP in the non-ischemic area ( NA ) , ischemic central area ( CA ) and BA, and markedly reduced the extent of dispersion of FRP of hearts in anesthetized cats. The results suggest that the antagonizing effect of Dau on the arrhythmias caused by acute myocardial ischemia and reperfusion might be related to its action of prolonging FRP and decreasing the dispersion of FRP in ischemic hearts.
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AIM To study sodium ferulute on monophasic action potential of ventricular muscle. METHODS Well being rabbits( n =20) were divided into 2 groups randomly,benzyltetrahydroplmatine(BTHP)group is a control group,the other is a study group. Franz's Quadrupole contact electrod catheter is advanced into the rigter ventricular by vein.MAP is recorded by traditional methods. At the same time Ⅱ lead ECG was recorded. Control group and study group were administered BTHP(5 mg?kg -1 ) and sodium ferulute(0 6 g?kg -1 ) respectively,before and after administration the duration of MAP at 20%(MAPD20),50%(MAPD50) and 90% (MAPD90) repolarization,amplitude of MAP (MAPA) and effective refractory period(ERP)were measured. RESULT In control group MAPD50,MAPD90 and ERP were significantly prolonged (124 5?8 96) ms vs (97 5?6 77) ms,(153?7 53) ms vs (123 5?5 8) ms,(142?13 37) vs (111?13 50) ms,respectively, P 0 05). CONCLUSION Sodium ferulute may be potassium channel blocker.