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Objective To evaluate the effects of dexmedetomidine on the electrophysiological stability of ventricular myocardium and the expression of gap junction connexin43 (Cx43) in rats in an in vitro experiment.Methods Healthy adult Sprague-Dawley rats of both sexes,weighing 270-330 g,were anesthetized with 3.0％ pentobarbital sodium 50 mg/kg.Their hearts were excised and retrogradely perfused in a Langendorff apparatus with K-H solution saturated with 95％ 02-5％ CO2 at 37 ℃.Twelve isolated rat hearts were divided into 2 groups (n =6 each) using a random number table:control group (group C) and dexmedetomidine group (group D).After 15 min of perfusion with K-H solution,hearts were continuously perfused for 30 min with K-H solution in group C or with K-H solution containing dexmedetomidine 50 ng/ml in group D.The monophasic action potential (MAP) and ventricular effective refractory period (VERP) of the left ventricular myocardium were recorded.Myocardial MAP duration at 90％ repolarization (MAPD90) and the ratio of VERP to MAPD9.(VERP/MAPD90) were calculated.Repetitive regular stimuli (S1) were followed by a single extrastimulus (S2),and the longest pacing cycle length of ventricular fibrillation threshold and development of ventricular arrhythmia were recorded.Left ventricular myocardial tissues were obtained for detection of the expression of myocardial Cx43 by Western blot.Results Compared with group C,the MAPD90 and VERP were significantly prolonged,VERP/MAPD90 ratio was decreased,the longest pacing cycle length of ventricular fibrillation threshold was prolonged,the incidence of ventricular arrhythmia was increased,and the expression of myocardial Cx43 was down-regulated in group D (P＜ 0.05).Conclusion Dexmedetomidine can decrease the electruphysiological stability of ventricular myocardium and down-regulate the expression uf Cx43,thus increasing the risk of arrhythmia in rats in an in vitro experiment.
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Objective To investigate the effect of dexmedetomidine on myocardial repolarization heterogeneity and the expression of Cx43 during ischemia-reperfusion and the role of Cx43 in the dexmedetomidine for inhibition of myocardial repolarization heterogeneity during ischemia-reperfusion in isolated rabbit hearts.Methods Eighteen healthy adult rabbits,weighing (2.0±0.5) kg,were randomly divided into three groups after Langendorff isolated heart perfusion model had been prepared and K-H fluid had been perfused and balanced 15 min.In the control group (group C),37℃ K-H fluid was continuously perfused and balanced for 150 min.In group IR,K-H fluid was stopped after perfusion continue filling for 15 min,and then made the cardiac stop for 60 min with the injection of Thomas solution 10 ml/kg while the heart was protected by the 4℃ Thomas solution around.Following the reperfusion of 4℃ Thomas solution 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 given (group DEX),dexmedetomidine was added in the K-H fluid and the Thomas solution 25 ng/ml.The other procedures were the same as those of group IR.The heart rate (HR),90% monophasic action potential duration (MAPD90) were recorded at the time of balance perfusion record 15 min (T0),continue perfusion 15 min/balance 30 min (T1),reperfusion 30 min/balance 120 min (T2) and reperfusion 60min/balance 150 min (T3).The transmural dispersion of repolarization (TDR) was calculated.To observe the cardiac reperfusion arrhythmia and rebeating time and recording.Detection expression of Cx43 in the left ventricular myocardial by Western blot and immunohistochemistry at T3.Results Group DEX cardiac resuscitation time was significantly shorter than that of group IR (P<0.05).In group DEX.Compared with T0,HR was significantly decreased and TDR was significantly increased in groups IR and DEX at T2、T3 (P<0.05).Compared with group IR,the TDR of group DEX was significantly decreased at T2、T3 (P<0.05).Compared with group C,the expression of Cx43 was decreased (P<0.05) and the distribution was not uniform in groups IR and DEX.Compared with group IR,the expression of Cx43 was decreased (P<0.05) and the distribution was improved in group DEX.Conclusion Dexmedetomidine could inhibits myocardial repolarization heterogeneity of ischemia-reperfusion injury,and thus play a stable cardiac conduction,reduce reperfusion arrhythmias,and its mechanism may be that dexmedetomidine could inhibits gap junctional uncoupling and inhibits expression and distribution of connexins decreased.
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Objective To evaluate efficacy of rotigaptide ZP123 on prevention of negative chronotropic effect caused by dexmedetomidine lengthening repolarization duration of the isolated rat hearts.Methods Eighteen healthy adult SD rats of either gender,weighing (300±30) g,were prepared isolated heart perfusion model by Langendorff.After 15 min perfusion and balance of K-H fluid,the isolated hearts were randomly divided into 3 groups (n=6 each): The hearts were continuously pefused for 30 min with 37℃ K-H solution in control group (group C),with dexmedetomidine 50 ng/ml in dexmedetomidine group (group D),or with rotigaptide 80 nmol/L combined with dexmedetomidine 50 ng/ml in rotigaptide combined with dexmedetomidine group (group ZD).In the whole Langendorff-perfused hearts,at the end of balanced infusion for 15 min (T0) and at 15(T1),30(T2) min of continued perfusion with K-H solution,the monophasic action potential (MAP) and heart rate (HR) were recorded from left anterior free wall,MAP duration at 50% repolarization (MAPD50) and at 90% repolarization (MAPD90),monophasic action potential amplitude (MAPA) and maximal velocity (Vmax) were calculated.Results Compared with T0,HR in group D was significantly declined at T1,T2;MAPD90 and MAPD50 in group D were significantly increased at T1,T2 (P<0.05).Compared with groups C and ZD,HR in group D was significantly declined at T1,T2;MAPD90 and MAPD50 in group D were significantly increased at T1,T2 (P<0.05).There was no significant difference in MAPA and Vmax between the three groups.Conclusion Rotigaptide antagonizes negative chronotropic effect induced by dexmedetomidine through shortening monophasic action potential duration in the myocardium of left ventricle of the isolated rat hearts.
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Objective To evaluate the effects of different target plasma concentrations of propofol on ventricular repolarization in elderly patients.Methods Forty-five patients,aged 65-80 yr,weighing 43-85 kg,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,scheduled for elective surgery under general anesthesia,were divided into 3 groups (n=15 each) using a random number table:propofol at target plasma concentration of 2 μg/ml group (group P1),propofol at target plasma concentration of 3 μg/ml group (group P2) and propofol at target plasma concentration of 4 μg/ml group (group P3).Before induction of anesthesia (T1) and at 5 min after propofol reached the target plasma concentration (T2),12-lead electrocardiogram was recorded,the QT and Tp-e intervals were measured,and the corrected QT (QTc) interval and Tp-e/QT ratio were calculated.Results There were no significant differences in QTc interval,Tp-e interval or Tp-e/QT ratio at T1,2 between the three groups (P＞0.05).Compared with those at T1,the QTc and Tp-e intervals were significantly shortened and the Tp-e/QT ratio was decreased at T2 in P1 and P2 groups,and the Tp-e interval was shorten and the Tp-e/QT ratio was decreased at T2 (P＜ 0.05),and no significant change was found in the QTc interval at T2 in group P3 (P＞0.05).Conclusion Propofol at clinically relevant concentrations can shorten the ventricular repolarization in elderly patients.
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Objective To evaluate the role of δ-opioid receptors in hydromorphone postcondition-ing-induced maintenance of electrophysiological stability during ischemia-reperfusion(I∕R)in isolated rat hearts. Methods Healthy male Sprague-Dawley rats, aged 2-3 months, weighing 280-360 g, were used in this study. The animals were anesthetized with intraperitoneal pentobarbital 60 mg∕kg. Their hearts were immediately removed and perfused in a Langendorff apparatus. Thirty-two isolated hearts were divided into 4 groups after successful preparation of Langendorff perfusion model(n=8 each)using a random number ta-ble: control group(group C), group I∕R, hydromorphone postconditioning group(group HP)and hydro-morphone plus δ-opioid receptor antagonist naltridole postconditioning group(group HNP). In HP and HNP groups, the hearts were perfused for 10 min with K-H solution containing 41 ng∕ml hydromorphone and 41 ng∕ml hydromorphone plus 5 μmol∕L naltridole, respectively, and then with K-H solution for 50 min. At 20 min of stabilization(T0)and 10, 25 and 60 min of reperfusion(T1-2), heart rate(HR), monophasic action potential(MAP)duration at 90% repolarization(MAPD90)of the two layers(endocar-dium, epicardium)of the anterior left ventricular wall were recorded. Transmural dispersion of repolariza-tion(TDR)was calculated. The development of arrhythmia, time for restoration of spontaneous heart beat and duration of arrhythmia were recorded during the period of reperfusion. Results Compared with group C, MAPD90of endocardium at T1-2and MAPD90of epicardium at T1were significantly prolonged in I∕R and HP groups, HR was significantly decreased at T2-3, MAPD90of endocardium and epicardium was prolonged at T1-3in group HNP, TDR was significantly enlarged at T1in group I∕R and at T2in group HNP, and TDR was decreased at T3in group HP(P<005). Compared with group I∕R, no significant change was found in arrhythmia score(P>005), the time for restoration of spontaneous heart beat was significantly shortened, and TDR was decreased at T1in HP and HNP groups, duration of arrhythmia was significantly shortened, and MAPD90of endocardium was shortened at T1in group HP, and HR was significantly decreased at T2-3, MAPD90of endocardium and epicardium was prolonged at T1-3, and TDR was decreased at T2-3in group HNP(P<005). Compared with group HP, no significant change was found in time for restoration of spon-taneous heart beat, duration of arrhythmia or arrhythmia score(P>005), HR was significantly decreased at T2-3, MAPD90of endocardium and epicardium was prolonged at T1-3, and TDR was increased at T3in group HNP(P<005). Conclusion The mechanism underlying hydromorphone postconditioning-induced maintenance of electrophysiological stability during I∕R is related to activating δ-opioid receptors in isolated rat hearts.
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Objective To evaluate the effect of hydromorphone postconditioning on the electrophysiological stability during ischemia-reperfusion (I/R) in isolated rat hearts.Methods Healthy adult male Sprague-Dawley rats,aged 2-3 months,weighing 280-360 g,were heparinized and anesthetized with pentobarbital sodium.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.Twenty-four Langendorff-perfused hearts were divided into 3 groups (n =8 each) using a random number table:control group (group C),I/R group and hydromorphone postconditioning group (group HM).The isolated hearts were subjected to 60 min ischemia followed by 60 min reperfusion to establish the model of isolated heart I/R injury.The isolated hearts were perfused with K-H solution containing 4.1 ng/ml hydromorphone for 10 min starting from onset of reperfusion in group HM.Heart rate,electrocardiogram,coronary flow,and monophasic action potential amplitude,in the left ventricular endocardium,mid-myocardium and epicardium the maximal increase rate (Vmax) at the 0 phase,and monophasic action potential duration at 50％ and 90％ repolarization (MAPD50 and MAPD90,respectively) were recorded at 20 min of stabilization (T0) and 10,25,40 and 60 min of reperfusion (T1-4).The transmural dispersion of repolarization (TDR) was calculated,and the time for restoratiou of spontaneous heart beat was recorded.Results There was no significant difference in the heart rate,coronary flow or monophasic action potential amplitude between the three groups (P＞0.05).Compared with group C,V in the epieardium was significantly decreased,MAPD50 and MAPD90 in the three transmural layers were prolonged,and TDR was prolonged in group I/R (P＜0.05).Compared with group I/R,the time for restoration of spontaneous heart beat,MAPD50 in the endoeardium and mid-myocardium,and MAPD90 and TDR in the endocardium were significantly shortened (P＜0.05),and no significant change was found in V in group HM (P＞0.05).Conclusion Hydromorphone postconditioning is helpful in maintaining the electrophysiological stability during I/R in isolated rat hearts.
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Objective To evaluate the effects of preoperative prophylactic infusion of cephalosporins antibiotics on electrocardiogram(ECG)during anesthesia induction with propofol. Methods Fifty female patients,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,aged 20-50 yr,weighing 43-75kg,scheduled for elective surgery,were divided into cefuroxime sodium group(group CEFU)and cefathiamidine group(group CEFA),with 25 patients in each group. After cefuroxime sodium was infused in group CEFU or cefathiamidine was infused in group CEFA,propofol was given by target-controlled infusion(plasma concentration 4 μg/ml).Before infusion of cefuroxime sodium or cefathiamidine,after completion of infusion and at 5min after propofol reached the target concentration,12-lead ECG was recorded,and mean arterial pressure and heart rate were simultaneously recorded. Tp-e interval and Tp-e/QT ratio were calculated.Results Compared with the baseline before infusion of cefuroxime sodium or cefathiamidine,Tp-e interval was significantly prolonged after completion of infusion and at 5min after propofol reached the target concentration in group CEFU,and Tp-e interval was significantly prolonged,and Tp-e/QT ratio was enlarged in group CEFA(P0.05).Conclusion Preoperative prophylactic infusion of cefuroxime sodium produces less ECG interference than preoperative prophylactic infusion of cefathiamidine during anesthesia induction with propofol.
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Objective To evaluate the effects of different concentrations of remifentanil on myocardial monophasic action potential (MAP) in isolated rabbit hearts.Methods Adult rabbits of both sexes,weighing 2.0-2.5 kg,were used in the study.Their hearts were excised,and retrogradely perfused with oxygenated K-H solution saturated with 95％O2-5％CO2 at 37 ℃ in a Langendorff apparatus.Twenty-four isolated hearts were randomly divided into 4 groups (n =6 each) using a random number table:control group (group C) and 3 different concentrations of remifentanil groups (group R1-3).After 15 min of stabilization,K-H solution was continuously perfused for 60 min in group C,and K-H solution containing 12,25 and 50 ng/ml remifentanil was continuously perfused for 60 min in R1,R2 and R3 groups,respectively.At 15 min of stabilization,and 15,30 and 60 min of perfusion with K-H solution,the heart rate,and the maximal velocity and amplitude of the MAP in the three layers of the left ventricular anterior wall were recorded,and the action potential duration at 90％ repolarization and transmural dispersion of repolarization (TDR) were calculated.Results Compared with group C,the heart rate was significantly decreased,and the action potential duration at 90％ repolarization and TDR were significantly prolonged at 15,30 and 60 min of perfusion in R1-3 groups (P＜0.05).Compared with C and R1 groups,the maximal velocity and amplitude of MAP were significantly decreased at 15,30 and 60 min of perfusion in R2 and R3 groups (P＜0.05).Conclusion Low-concentration remifentanil induces heart block through increasing TDR,however,high-concentration remifentanil induces heart block through inhibiting myocardial MAP depolarization and increasing TDR in the isolated rabbit hearts.
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Objective To evaluate the effects of different concentrations of remifentanil on the expression and distribution of gap junction protein connexin 43 (Cx43) in the cardiomyocytes of rabbits.Methods Healthy adult rabbits of both sexes,weighing 2.0-2.5 kg,were anesthetized with pentobarbital sodium.Their hearts were rapidly excised and retrogradely perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.After 15 min of stabilization with K-H solution,the 24 isolated hearts were randomly divided into 4 groups (n =6 each) using a random number table:control group (group C),and low,medium and high concentrations of remifentanil groups (R1-3 groups).The hearts were continuously perfused with K-H solution at 37 ℃ in group C.The hearts were perfused for 60 min with K-H solution containing remifentanil 12,25 and 50 ng/ml in R1-3 groups,respectively.The myocardial specimens were then obtained from the anterior wall of the left ventricle for detection of the expression and distribution of Cx43 by Western blot and immunohistochemistry,respectively.Results The expression of Cx43 was gradually down-regulated in C and R1-3 groups in turn (P＜0.05).Compared with group C,there was a tendency for the proteins localized at end-to-end contact sites of ventricular cardiomyocytes to localize at side-to-side contact sites in R1-3 groups,and the distribution was messy in R1-3 groups.Conclusion Remifentanil dose-dependently down-regulates the expression of Cx43 and changes the distribution of Cx43,which may be one of the mechanisms of remifentanil-induced arrhythmia in rabbits.
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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 investigate the role of potassium channel in remifentanil-induced prolongation of monophasic action potential duration (MAPD) in the myocardium of rabbits.Methods Eighteen adult rabbit hearts successfully perfused in a Langendorff apparatus were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),remifentanil group (group R),and K+ channel blocker tetraethylammonium group (group T).After 15 min stabilization with K-H solution,group C was continuously perfused with K-H solution for 60 min,and R and T groups were perfused with KH solution containing 12 ng/ml remifentanil and 10 ng/ml tetraethylammonium,respectively,for 60 min.At 15 min of stabilization,and 15,30 and 60 min of perfusion,heart rate,MAPD of all the three layers of the myocardium in the anterior wall of the left ventricular was recorded.MAPD at 50％ and 90％ repolarization (MAPD50,MAPD90) were calculated.Results Compared with group C,heart rate was significantly decreased,MAPD50 and MAPD90 were prolonged in R and T groups (P ＜0.05).Conclusion The mechanism by which remifentanil prolongs MAPD in the myocardium of rabbits is associated with blockade of the potassium channels.
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Objective To investigate the effects of target-controlled confusion of propofol with different concentrations on ventricular repolarization after prophylactic infusion of cefuroxime sodium. Methods Sixty ASA physical status Ⅰ or Ⅱ female patients,aged 18-65 years,undergoing elective gynecological surgery were randomly divided into three groups:group P2 (n =20)with TCI 2 μg/ml, group P3 (n =1 9)with TCI 3 μg/ml and group P4 (n =20)with TCI 4 μg/ml.Firstly,they were re-hydrated;secondly,the patients in groups P2,P3 and P4 were intravenous infused with cefuroxime sodium 2.5 g (in 100 ml normal saline)and then target-controlled infused of propofol 2 μg/ml,3μg/ml and 4 μg/ml in target plasma concentration,respectively.At three pionts of time:after rehy-dration before intravenous antibiotics (T0 ),after intravenous antibiotics before TCI of propofol (T1 ), after TCI of propofol (T2 ),QT interval,QTc interval,Tp-e interval were measured and recorded, respectively.Results Compared with T0 ,QTc [(469.9 ± 34.0)ms vs.(451.2 ± 24.9)ms],Tp-e [(107±25)ms vs.(94±20)ms]and Tp-e/QT (0.260±0.058 vs.0.236±0.043)in group P4 were sig-nificantly prolonged at T1 (P < 0.05 ).Compared with T1 ,QTc of groups P2 [(437.4 ± 24.4)ms vs. (453.3±28.0)ms]and P4 [(438.8±29.9)ms vs.(469.9±34.0)ms]were shortened significantly at T2 (P <0.05).Conclusion Propofol could improve ventricular reporlarization heterogeneity caused by cefu-roxime sodium.
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Objective To investigate the effects of hypothermia combined with dexmedetomidine on myocardial monophasic action potentials (MAPs) in isolated rabbit hearts.Methods Adult rabbits,weighing 2.0-2.5 kg,were heparinized and anesthetized with pentobarbital sodium 30 mg/kg.Their hearts were rapidly removed and retrogradely perfused in a Langendorff apparatus at 37 ℃.Eighteen hearts were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),hypothermia group (group H),and hypothermia+dexmedetomidine group (group HD).The hearts were continuously perfused for 60 min with 37 ℃ K-H solution in group C,with 32 ℃ K-H solution in group H,or with 32 ℃ K-H solution containing dexmedetomidine 25 ng/ml in group HD.At the end of equilibration (T0) and at 15,30 and 60 min of perfusion with K-H solution,HR and MAPs of left ventricular epicardium,mid-myocardium and endocardium were recorded.MAP duration at 50％ repolarization (MAPD50) and at 90％ repolarization (MAPD90),monophasic action potential amplitude (MAPA) and maximal velocity (Vmax) were calculated.Results Compared with group C,HR was significantly decreased,and MAPD50 and MAPD90 were prolonged at each time of perfusion with K-H solution in H and HD groups.There was no significant difference in HR,MAPD50 and MAPD90 between H group and HD group.There was no significant difference in MAPA and Vmax between the three groups.Conclusion Hypothermia combined with dexmedetomidine can lead to prolongation of myocardial repolarization,and dexmedetomidine exerts no effect on hypothermia-induced change in MAPs in isolated rabbit hearts.
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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 evaluate the effect of fluoride on the viability of rat ameloblast HAT-7 cells and calcium concentration in the cells.Methods:HAT-7 cells were exposed to NaF at 0,0.4,0.8,1.6,3.2 and 6.4 mmol/L for 24,48 and 72 h respectively. CCK-8 assay was performed to examine the cells proliferation;the apoptosis rate was determined by flow cytometry;Ca2 +concentration in the cells was detected by laser scanning confocal microscopy.Results:The cell proliferation was increased by NaF at 0.4 mmol/L and 0.8 mmol/L,whereas inhibited at 1.6 mmol/L and above.The effects were in a time-dependent manner.NaF increased apoptosis of the cells and increased Ca2 + concentration in the cells in a concentration-dependent manner.Conclusion:Fluoride at low doses promotes proliferation,at high doses inhibits proliferation of HAT-7 cells.NaF of 1.6 mmol/L or more induces apoptosis of HAT-7 cells and in-duce Ca2 + overloading in the cells.
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<p><b>OBJECTIVE</b>To study the effect of excessive fluoride on calcium overload and apoptosis in cultured rat ameloblasts in vitro.</p><p><b>METHODS</b>Logarithmic-phase ameloblasts (HAT-7) were treated with 0, 0.4, 0.8, 1.6, 3.2, and 6.4 mmol · L(-1) sodium fluoride (NaF) solution. Cell activities were detected by using a Cell Counting Kit 8 (CCK-8) assay after 48 h of treatment. The effect of fluoride on cell apoptosis was analyzed by using flow cytometry. Excessive fluoride-induced calcium concentration and calreticulin expression changes in ameloblasts were detected by using laser scanning confocal microscopy, Western blot analysis, and real-time quantitative polymerase chain reaction.</p><p><b>RESULTS</b>NaF inhibited ameloblast activity at 1.6, 3.2, and 6.4 mmol · L(-1) (dose-dependent) after 48 h of induction. The Ca2+ fluorescence intensity of HAT-7 cells incubated with 1.6 and 3.2 mmol · L(-1) NaF was higher than that in the control group. The fluoride-induced early-stage apoptosis of ameloblasts after 48 h of induction and the early-stage apoptosis rate was positively correlated with fluoride concentration. Calreticulin mRNA expression in HAT-7 cells was higher than that in the control group after 48 h of incubation with 0.8, 1.2, and 1.6 mmol · L(-1) NaF.</p><p><b>CONCLUSION</b>Excessive fluoride-induced calcium overload in ameloblasts and further caused endoplasmic reticulum stress-mediated apoptosis.</p>