Objective To investigate the changes in TNF? content of sciatic nerve induced by chronic constriction injury (CCI) of sciatic nerve to determine the role of TNFa in the development of neuropathic pain. Methods Eight-four female health SD rats weighing 250-300g were anesthetized with sodium barbiturate. Unilateral sciatic nerve was exposed and ligated at the middle of thigh. Three ligatures (chromic catgut 4.0) were placed around the sciatic nerve and tied. The distance between the two ligatures was about 1 mm. Sham operation was performed on the contralateral thigh. The sciatic nerve was exposed and mobilized but not ligated. The thermal nociceptive threshold was determined by measuring the withdrawal latency of hindpaw placed on a 58℃ hot plate on days 0.5, 1, 3, 5, 7, 9, 11, 13 and 14 after surgery. Animals were sacrificed on days 0.5, 1, 3, 7, 10 and 14 after surgery. Sciatic nerves were removed from both thighs and frozen at - 80℃ for determination of TNF? content. Sciatic nerve from healthy animals was used as control. The percentage of maximal possible response (% MPR) , was determined for each group (CCI, sham operation, control) % MPR= (new withdrawal latency- average baseline latency)/( 15-average baseline latency) . The distribution of TNF? between supernatant and sediment was also determined. Results The average baseline nociceptive threshold (withdrawal latency) was (7.9?0.2)s. There was significant different in %MPR between the two hindpaws on days 1, 3, 5, 7, 9 and 11 after surgery. The TNF? content of sciatic nerve from healthy rats was (40.62? 0.24) pg/mg protein. The TNF? content of the ligated sciatic nerve was elevated abruptly in 12h after ligation, then abruptly declined to a plateau but was still significantly higher than that of sham-operated side on days 1 and 3. There was no significant difference in TNF? content of sciatic nerve between control group and sham-operation group. The relative content of TNF? content in the sediment of ligated sciatic nerve gradually increased and reached the peak on day 7 and then gradually decreased. Conclusion The TNF? content of peripheral nerves plays an important role in the development of neuropathic pain. Membrane-combined TNF? is involved in the process of nerve repairing.

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.

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.

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.

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.

Objective To investigate the clinical effects of transurethral resection of cystitis after gynecological cystitis after transurethral resection of bladder,and to observe the effect on patients' anxiety(SAS)and quality of life index(QOL).Methods The clinical data of 62 patients with cystitis glandularis admitted to hospital from January 2011 to December 2016 were retrospectively analyzed.The control group was treated with plasma ablation alone,with plasmakinetic resection of Kangfuxin liquid combined with gemcitabine intravesical therapy as the treatment group,31 cases in each group.Statistics of two groups of patients with clinical efficacy,followed up for 12 months,and the anxiety self-rating scale(SAS)was used to evaluate the anxiety of the two groups before and after treatment,QOL was used to evaluate the quality of life before and after treatment in two groups of patients.The recurrence rate of two groups were recorded.Results After treatment,the effective rate of the treatment group was 80.65％,slightly higher than the control group 77.42％,the difference was statistically significant(P<0.05),the SAS score in the treatment group was slightly higher than before treatment,but the difference was not statistically significant,the SAS score in the control group was significantly lower than before treatment,after treatment between the groups,the difference was statistically significant(P<0.05).The QOL index of the treatment group decreased slightly after treatment,but the difference was not statistically significant.The QOL index of the treatment group decreased significantly after treatment,and compared between the two groups after treatment,the difference was statistically significant(P<0.05).Follow-up of 12 months,the relapse rate in the treatment group was 11.11％,slightly lower than the control group 18.75％,the difference was statistically significant(P<0.05).Conclusion Compared to pure plasmapheresis,the use of postoperative intravesical instillation of bladder irrigation with the same effect,but the latter may increase the degree of anxiety in patients,thus affecting the quality of life of patients,so for the non-mandatory use of drugs treatment,surgery may be given priority to surgery alone.

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.

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.

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.

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.