Lappaconitine (LA) is a diterpene alkaloid isolated from Aconitum species and has been used in traditional Chinese medicine as an analgesic. Previous studies have also suggested that LA exerts anti-inflammatory and immunomodulatory effects. Neuroinflammation and oxidative stress, both of which are associated with mitochondrial dysfunction and apoptosis, contribute to the development and maintenance of neuropathic pain. We hypothesized that LA may protect SH-SY5Y cells against inflammation- and apoptosis-associated injury. To investigate whether LA attenuates TNF-α-induced inflammatory injury and apoptosis in SH-SY5Y cells and to explore the potential mechanisms involved. SH-SY5Y cells were pretreated with LA (0.1 or 1 μM) for 24 h and subsequently exposed to TNF-α (10 ng/mL) for 12 h. Apoptosis, mitochondrial function, inflammatory cytokine production, and the expression of mitophagy-related proteins were assessed in LA-pretreated and non-pretreated cells. LA pretreatment (0.1 or 1 μM) reduced apoptosis in TNF-α-exposed SH-SY5Y cells, increased Bcl-2 expression, and decreased the expression of Bax, Caspase-3, and Caspase-9. LA pretreatment also suppressed NF-κB activation and reduced IL-1β and IL-6 production. In addition, LA preserved mitochondrial integrity, as indicated by maintenance of mitochondrial membrane potential, reduced cytochrome c release, and decreased ROS accumulation. The expression of the mitophagy-related proteins PINK1 and Parkin was also increased following LA pretreatment. LA attenuated TNF-α-induced inflammatory injury and apoptosis in SH-SY5Y cells. These protective effects were associated with modulation of apoptosis-related signaling, suppression of inflammatory responses, preservation of mitochondrial function, and increased expression of PINK1/Parkin-related proteins. These findings suggest that LA may exert neuroprotective effects under inflammatory conditions.

Background Patients with insomnia may exhibit altered pharmacodynamics to anesthetics. This study aimed to explore the changes in propofol dosage in patients with insomnia undergoing digestive endoscopy, compared to patients with normal sleep patterns. Methods A multicenter prospective cohort study was conducted. Propensity score matching (1:3) was applied to balance baseline characteristics. The primary outcome was the total propofol consumption during digestive endoscopy, and gender/age/BMI subgroup analysis was performed. The secondary outcome included the propofol dosage required for successful endoscopic insertion and gender/age/BMI subgroup analysis, the recovery time, the correlation between propofol dosage requirements and insomnia severity, as well as perioperative adverse events. Results After matching (140 patients in the insomnia group vs 420 patients in the normal sleep group), the insomnia group required significantly higher total propofol consumption (3.8 ± 0.8 vs 3.3 ± 0.6 mg/kg, P = 0.003) and propofol dosage required for successful endoscopic insertion (2.4 ± 0.3 vs 2.1 ± 0.3 mg/kg, P = 0.043). Subgroup analyses of total propofol consumption and propofol dosage required for successful endoscopic insertion confirmed these findings across gender and age. The recovery time and the incidence of perioperative adverse events were comparable in both groups. A positive correlation was observed between propofol dosage and insomnia severity (P < 0.001). Conclusions Patients with insomnia require higher propofol dosages during digestive endoscopy, suggesting the need for individualized anesthesia protocols in this population. Trial registration: ClinicalTrials.Gov (NCT06376760, Principal investigator: Fang Luo, Date of registration: 17 April, 2024)

Lidocaine nebulization is noninvasive, safe, and easy to perform. However, it does not provide adequate anesthesia due to the following reasons: 1. There is a high wastage of lidocaine aerosol, with at least 70 % of the lidocaine aerosol being lost from the cannula. This loss of lidocaine results in a lower amount of inhaled lidocaine, which is insufficient to provide adequate anesthesia. 2. The commercial lidocaine preparation has a low penetrating potency. The onset of anesthesia is directly related to the amount of local anesthetic in the lipidsoluble form. However, there are only a few lipid-soluble prototypes in the commercially available lidocaine cartridges. This is because the lidocaine is purposely formulated as acidic solutions (with pH levels between 3.5 and 5.5) in order to enhance the solubility and stability of the anesthetic salts. To address these issues and improve lidocaine anesthesia potency while reducing wastage, a "Y" type cannula was used for aerosol inhalation. Additionally, 1/5 vol of 5 % sodium bicarbonate solution was added to 2 % lidocaine to enhance the pH value to 7.2. This alkalized lidocaine nebulization provides an effective topical anesthesia for bronchoscopy.

Objective:To investigate the effects of eucommia extract on immune function and TLR2/NF-κB/TNF signaling pathway in rats with rheumatoid arthritis. Methods:A total of 35 SD rats were divided into the control group（CG）,rheumatoid arthritis rat model group（MG）,model rats treated with eucommia extract low-dose（EELD）group,model rats treated with methotrexate intervention（EEMD）group,and model rats were treated with eucommia extract high-dose（EEHD）group,with 7 rats in each group. The degree of joint swelling and joint index score were recorded. Serum immunoglobulin levels were detected by ELISA. The level of T lymphocytes was detected by flow cytometry. HE staining was used to observe joint lesions. The protein expressions of TLR2,NF-κB and TNF in the synovial tissue of ankle joint were detected by Western blotting. Results:Compared with the CG group,the left hind foot swelling degree,joint index score,immunoglobulin water,TLR2,NF-κB,TNF-αand CD4+ and CD4+CD25+Treg levels of the MG group were increased,and the levels of CD4+ and CD4+CD25+Treg were decreased（P ＜ 0.05）. The left hind foot swelling degree,joint index score,immunoglobulin water,TLR2,NF-κB and TNF-α of rats in the EELD,EEMD and EEHD groups were decreased,while CD4+ and CD4+CD25+Treg levels were increased（P ＜ 0.05）. There was no significant difference between the EELD and EEMD groups（P ＞ 0.05）. Compared with the EEMD group,the left hind foot swelling degree,joint index score,immunoglobulin water,TLR2,NF-κB,TNF-α were decreased,and CD4+ and CD4+CD25+Treg levels were increased（P ＜ 0.05）.Conclusion:Eucommia extract may play a protective role by regulating the levels of serum immunoglobulin and T lymphocytes,inhibiting the TLR2 and NF-κB signaling pathways in rheumatoid arthritis,reducing the inflammatory level and improving rheumatoid arthritis.

Objective In order to evaluate the role of β-adrenergic receptor in bupivacaine induced cardiac depression, contractility of bupivacaine infused ventricular myoctes was assessed by a video-based edge-detection system in the presence and absence of isoproterenol, with and without β1 adrenergic antagonist esmolol. Methods We isolated the rat ventricular myocyte by enzymatic hydrolysis.The cardiomyocytes were randomly divided into 3 groups: bupivacaine group, isoproterenol + bupivacaine group and isoproterenol + esmolol + bupivacaine group.The cells contractile function（dep v, bl % peak h and time to peak 50%） were continually monitored and recorded when the cells perfused with the solution describe above. Results Bupivacaine concentration dependently suppresses myocardial contraction function.Low-concentration bupivacaine（5.9 and 8.9 μmol/L） do not suppress myocardial contractility, however, high-concentration bupivacaine suppress myocardial contraction function.Isoproterenol enhances myocardial contractility in the presence of bupivacaine（5.9 and 8.9 μmol/L）,but inhibits cardiac contraction in the presence of high-concentration bupivacaine（13.3 μmol/L）.Isoproterenol reduced the median effective dose of bupivacaine-induced myocardial contraction failure.The EC50（95%CI） of bupivacaine was 44.9（33.9～55.4） μmol/L in bupivacaine group.The EC50（95%CI） of bupivacaine was 17.9（5.9～28.9） μmol/L in isoproterenol + bupivacaine group, and significantly lower than bupivacaine group（P＜0.05）.β1-adrenergic inhibitors can reverse the effect of Isoproterenol.Addition of esmolol enhanced EC50（95%CI） of bupivacaine from 17.9（5.9～28.9） μmol/L to 40.6（28.4～53.7） μmol/L（P＜0.05）.Bupivacaine induced contractile depression is reversible. Conclusion Bupivacaine concentration dependently and reversibly suppresses myocardial contraction function.β1-adrenergic agonists can significantly increased bupivacaine-induced cardiotoxicity in rats, and β1-adrenergic inhibitors can reverse the effect of β1-adrenergic agonists.

Unicompartmental knee arthroplasty (UKA) is an ideal surgical approach in treatment of end-stage knee osteoarthritis (KOA), however, indications of UKA have been controversial, and the radiographic and symptomatic patellofemoral osteoarthritis (PFOA) are often considered as a contraindication of medial UKA. 337 fixed bearing UKAs were retrospectively recruited in our joint center between January 1, 2011 and June 30, 2020. There were 105 patients accompanied by PFOA and 232 patients have normal PF joint. International Cartilage Repair Society (ICRS) system was introduced to quantify the degeneration degree of PF joint. Oxford Knee Score (OKS), Forgotten Joint Score (FJS), Kellgren-Lawrence (K-L) classifying system and visual analogue scale (VAS) were adopted to evaluate outcomes between with and without PFOA. There was no significant difference of age, BMI, gender, OKS, FJS and other variables between PFOA and Non-PFOA group. After more than 5 years follow-up, UKA patients with or without PFOA could all achieve a satisfactory improvement of OKS, VAS and FJS score. ROM of the replaced knee increased from preoperative 110° to 130°. 74.3% (78/105) and 75.0% (174/232) patients have no change of K-L grade in PFOA and Non-PFOA group, OKS, FJS, VAS score and ROM were also comparable in all patients and no significant outcomes difference were found between two group. The presence of patellofemoral joint osteoarthritis and anterior knee pain should not be considered to be contraindications to medial fixed-bearing UKA.

Patellar resurfacing (PR) and peripheral patellar denervation (PD) are common surgical treatments for knee osteoarthritis (KOA) in total knee arthroplasty (TKA). The aim of study was to compare preventive effect on postoperative anterior knee pain (AKP) between PR and peripheral PD in TKA. A total of 202 patients who underwent unilateral TKA were randomized into 3 groups: T, TPD, and TPR. Patients in T group received simple TKA, patients in TPD group received TKA combined PD while patients in TPR group received TKA combined PR. Incidence, intensity, and presentation time of AKP and clinical outcomes were evaluated at 3, 6, 9, 12, 18, and 24 months postoperatively. The incidence of AKP was significantly lower and the intensity of AKP and patients’ satisfaction score were significantly better at 3 months after surgery in group TPD and TPR compared with group T. Compared with group TPR, the intensity of AKP was significantly better at 3 months after surgery in group TPD. There were no significant difference in Oxford knee score, range of motion (ROM), patellar score, knee society score (KSS) and activities of daily living (ADL) score among 3 groups in the follow-up period. Both PD and PR can effectively reduce the intensity and incidence of AKP after TKA and improve patients’ satisfaction at 3 months after TKA. Additionally, PD is more effective on alleviating AKP than PR.

目的 探讨右美托咪定拮抗阿霉素对小鼠心脏毒性的效果及作用机制.方法 100只清洁级雄性昆明种小鼠随机分为对照组(C组)和实验组(D组)各50只,每组又各分5个亚组,均一次性腹腔注射不同剂量阿霉素.C组每天腹腔注射0.9％氯化钠注射液0.005 mL·g-1,D组每天腹腔注射右美托咪定30μg·kg-1,共10 d.记录小鼠死亡数量,采用Probit法计算阿霉素致小鼠死亡的半数致死量(median lethal dose,LD50)及95％可信区间(95％CI).注射0.9％氯化钠/右美托咪定10 d后处死存活小鼠,电镜及光镜下观察小鼠心肌细胞组织学改变,免疫组化法测定小鼠心肌细胞bax和bcl-2蛋白表达情况.结果 C组阿霉素对昆明种小鼠腹腔给药的LD50为21.17 mg·kg-1(95％CI:18.12～24.74 mg·kg-1),D组LD50为29.18 mg·kg-1(95％CI:24.90～34.18 mg·kg-1),D组LD50显著高于C组(U=15.5,P=0.002).C组心肌细胞线粒体结构损伤较D组严重,且可见自噬小体.与C组比较,D组bax表达显著降低(χ2=25.90,P=0.000),2组bcl-2表达比较差异无统计学意义(P>0.05).结论 右美托咪定可明显提高阿霉素致小鼠死亡的LD50,提高小鼠生存率,其机制可能与右美托咪定降低心肌细胞线粒体损伤、抑制bax蛋白表达有关.

The new papers of phantom limb pain were reported in this yearbook, including altered cortical reorganization and brain functional connectivity in phantom limb pain, continuous peripheral nerve block to treat postamputation phantom limb pain.

Abstract The authors have requested that this preprint be removed from Research Square.

The diagnostic and therapeutic experiences of one chronic hepatitis B patient with hypophosphoric osteomalacia induced by low dosage oral adefovir dipivoxil for a long term were retrospectively analyzed. The patient primarily complained lumbago with gradual bilateral lower limb weakness. The patient had a history of a low dose adefovir dipivoxil orally for 6 years (10 mg/d), and manifested low blood phosphorus, high alkaline phosphatase and renal glycosuria, and abnormal function of proximal renal tubules in the examination. In view of previous medication history, adefovir dipivoxil was considered to be the cause of renal damage. Adefovir dipivoxil was replaced by entecavir dispersive tablets, and potassium, phosphorus, ossified triglyceride and other treatments were given. After that, the painful symptoms were obviously relieved and the indexes of blood phosphorus and renal glycosuria improved significantly. The experience of diagnosis and treatment for the patient were summarized and the relevant literatures were reviewed for the reference of clinicians.

The new progresses of phantom limb pain were reviewed, including therapy with selective nerve root injection of ozone, relationship between phantom limb pain and amputation reasons, anesthesia methods during surgery, peripheral nerve input or white matter changes after amputation.

At present, phantom limb pain (RLP) is still a very significant problem after amputation and their causes are only partially known. The treatment of phantom limb pain is also unsatisfactory. This paper summarized the research on phantom limb pain in the past one year, including mirror therapy, virtual integrated environment therapy, transcranial stimulation, cortical stimulation therapy, semicircular canal stimulation therapy, the study of predictive factors before and after phantom limb operation. Key words: Phantom limb; Neuralgia

Objective To research the effects of β-adrenoceptor agonists, isoproterenol and epinephrine, on electrocardiogram and myocardial mechanics in rats with bupivacaine poisoning. Methods Forty-two adult male SD rats were randomly divided into two parts. Each part was then divided into three groups: bupivacaine+saline group (group BS), bupivacaine+isoproterenol group (group BI) and bupivacaine+epinephrine group (group BE), 7 rats in each group. The rats were anesthetized intraperitoneal with 10% chloral hydrate. After bupivacaine was intravenously infused at 0.75 mg·kg-1·min-1 for 12 minutes and 40 seconds, 0.4 ml of normal saline, or isoproterenol (0.08 mg/kg), or epinephrine (6 μg/kg or 3 μg/kg) was caudal intravenously injected. In part one, electrocardiogram was continually monitored to analyze and record the duration of PR, QRS and heart rate. In part two, ventricular pressure waveform was monitored and left ventricular hemodynamic variables were continually recorded. Results Prolonged PR interval, widened QRS interval and decreased heart rate were observed in myocardium intoxicated by bupivacaine (all P<0.05). The effects of isoproterenol and epinephrine on PR interval and QRS interval in myocardium intoxicated by bupivacaine could not be observed markedly. When isoproterenol and epinephrine were injected intravenously respectively for 1 minute, the heart rate increased rapidly in the two groups (all P<0.05). However, there was no difference of the monitoring point after 1 minute. Bupivacaine could reduce left ventricular systolic pressure (LVSP), increase left ventricular end-diastolic pressure (LVEDP), decrease maximum rate of left ventricular pressure rise (+dp/dt max) and maximum rate of decrease of left ventricular internal pressure (-dp/dt max), and the results were statistically significant (all P<0.05) . Isoproterenol and epinephrine could aggravate the inhibitory effect of bupivacaine on myocardial, as a result of reduced LVSP and +dp/dt max. The inhibitory effects in the other two groups were statistically significant at 3 minutes after administration as well as other time points compared with group BS. But there was no significant effect on LVEDP and -dp/dt max. Conclusion Bupivacaine can depress myocardial conduction and left ventricular function in rats. β-adrenoceptor agonists such as isoproterenol and epinephrine can significantly aggravate bupivacaine-induced cardiotoxicity on left ventricular function. β-adrenoceptor agonists have no effect on bupivacaine-induced conductional toxicity in rats. However, they can improve the myocardial autorhythmicity of bupivacaine-induced. Key words: Isoproterenol; Epinephrine; Bupivacaine; Drug toxicity; Myocardium; Electrocardiography

Purpose: To investigate the analgesic effect of alkalized lidocaine on wound dressing operation in burn patients. Methods: 160 burn patients were divided into intervention group (N = 80) and control group (N = 80). The control group was treated with routine burn dressing, and the intervention group was sprayed with a 10: 1 configuration of 2% lidocaine and 5% sodium bicarbonate mixture spray. The heart rate (HR), peripheral oxygen saturation (SpO(2)), and pain (assessed using a visual analog scale [VAS]) were recorded 10 min before, during, and 10 min after debridement and dressing. The simplified version of the McGill pain questionnaire (SF-MPQ) was used to evaluate pain level. Results: The HR in the intervention group was significantly lower than that in control group (P < 0.001). The SpO(2) during the debridement and dressing in the intervention group was significantly higher than that in the control group (P < 0.001). The intervention group showed significantly lower VAS scores than control group (P < 0.001), and the pain sensation scores and pain scores during and after the debridement and dressing in the intervention group were significantly lower than those in the control group (P < 0.001). Conclusion: Alkalized lidocaine has significant analgesic and sedative effects during debridement and dressing of burn wounds, and it can relieve the anxiety and fear in burn patients, making patients relaxed and more amenable to undergo the debridement treatment.

Objective To investigate the effect and mechanism of isoprenaline,a β1-adrenergic receptor agonist,on mitochondrial edema of cardiomyocytes induced by bupivacaine.Methods Six healthy pathogen-free male SD rats,weighing 180-220 g,were received enzymatic hydrolysis separation for myocardial cells,which were randomly divided into 4 groups:physiological saline group (control group),bupivacaine group,bupivacaine+ isoprenaline group,and bupivacaine+ isoprenaline +esmolol group.The myocardial cells were electrically stimulated to induce rhythmic contraction for 60 s.Electron microscopy of myocardial mitochondria was performed to assess the damage of the structure.The amount of mitochondrial reactive oxygen species (ROS) was quantitatively measured by ROS assay kit in the above cardiomyocytes.(Repeat 3 times and take the average).Results The mitochondrial edema score and ROS production was significantly higher in bupivacaine group than those in control group (4 719.95 vs.3 921.94) (all P＜0.05).The extent of myocardial mitochondrial edema and ROS production were significantly higher in bupivacaine +isoprenaline group than those in bupivacaine group (5 192.25 vs.4 719.95) (all P＜0.05).The mitochondrial edema score and ROS production was significantly lower in bupivacaine + isoprenaline + esmolol group than those in bupivacaine + isoprenaline group (4 709.68 vs.5 192.25) (all P＜0.05).Conclusion The excitation of β31-adrenergic receptor induced by isoprenaline can interfere with mitochondrial metabolism and aggravate mitochondrial edema of cardiomyocytes caused by bupivacaine.

In order to determine the role of the adrenergic system in bupivacaine-induced cardiotoxicity, a series of experiments were performed. In an animal experiment, male Sprague-Dawley (SD) rats under chloral hydrate anesthesia received intravenous bupivacaine, followed by an intravenous injection of adrenalin or isoprenalin, and the electrocardiogram (ECG), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximum rate of rise of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease (-dP/dtmax) were continually monitored. In a cellular experiment, freshly isolated adult SD rat ventricular myocytes were perfused with bupivacaine at different concentrations in the presence or absence of isoprenalin, with or without esmolol. The percentage of the sarcomere shortening (bl% peak h), departure velocity (dep v) of sarcomere shortening and time to 50% of the peak speed of myocyte contraction (Tp50) was assessed by a video-based edge-detection system. In an additional experiment, Swiss mice pretreated with saline, isoprenalin, esmolol or dexmedetomidine received bupivacaine to determine the 50% lethal dose (LD50) of bupivacaine. Electron microscopy of myocardial mitochondria was performed to assess damage of these structures. To test mitochondrial reactive oxygen species (ROS) production, freshly isolated SD rat ventricular myocytes were incubated with bupivacaine in the presence of isoprenalin, with or without esmolol. First, our results showed that bupivacaine significantly reduced the LVSP and +dP/dtmax, as well as enhanced the LVEDP and -dP/dtmax (P < 0.05, vs. control, and vs. baseline). Adrenalin and isoprenalin induced a further reduction of LVSP and +dP/dtmax (P < 0.05, vs. before adrenalin or isoprenalin delivery, and vs. control). Second, bupivacaine induced a dose-dependent cardiomyocyte contractile depression. While 5.9 μmol/L or 8.9 μmol/L of bupivacaine resulted in no change, 30.0 μmol/L of bupivacaine prolonged the Tp50 and reduced the bl% peak h and dep v (P < 0.05, vs. control and vs. baseline). Isoprenalin aggravated the bupivacaine-induced cardiomyocyte contractile depression, significantly prolonging the Tp50 (P < 0.05, vs. bupivacaine alone) and reducing the dep v (P < 0.05, vs. bupivacaine alone). Third, esmolol and dexmedetomidine significantly enhanced, while isoprenalin significantly reduced, the LD50 of bupivacaine in mice. Fourth, bupivacaine led to significant mitochondrial swelling, and the extent of myocardial mitochondrial swelling in isoprenalin-pretreated mice was significantly higher than that compared with mice pretreated with saline, as reflected by the higher mitochondrial damage score (P < 0.01). Meanwhile, esmolol pretreatment significantly reduced the mitochondrial damage score (P < 0.01). Fifth, bupivacaine significantly increased the ROS in freshly isolated cardiomyocytes, and added isoprenalin induced a further enhancement of ROS production (P < 0.05, vs. bupivacaine alone). Added esmolol significantly decreased ROS production (P < 0.05, vs. bupivacaine + isoprenalin). Our results suggest that bupivacaine depressed cardiac automaticity, conductivity and contractility, but the predominant effect was contractile dysfunction which resulted from the disruption of mitochondrial energy metabolism. β-adrenergic activation aggravated the cellular metabolism disorder and therefore contractile dysfunction.

目的 观察盐酸纳布啡复合丙泊酚用于门诊人工流产术的疗效、术后镇痛效果及安全性.方法 选择ASAⅠ～Ⅱ级人工流产者120例,按随机数字表法分为对照组和试验组,每组60例.试验组静脉注射盐酸纳布啡0.2 mg/kg(稀释至2 mL),1 min后静脉注射丙泊酚2.0mg/kg;对照组静脉注射生理盐水2 mL,1 min后静脉注射丙泊酚3.0mg/kg.观察2组麻醉效果、术中丙泊酚用量、苏醒时间、术后5 min和30 min子宫收缩疼痛评分以及不良反应,记录人工流产者入室时(T0)、睫毛反应消失时(T1)、手术开始时(T2)、手术结束时(T3)及术后5 min时(T4)的收缩压(systolic blood pressure,SBP)、舒张压(diastolic blood pressure,DBP)、心率(heart rate,HR)及脉搏血氧饱和度(pulse oxygen saturation,SpO2).结果 2组SBP、DBP呈先降低再高升的趋势,时点间差异有统计学意义(P＜0.05),组间、组间·时点间交互作用差异无统计学意义(P＞0.05).2组HR呈先降低再高升的趋势,时点间、组间·时点间交互作用差异有统计学意义(P＜0.05),组间差异无统计学意义(P＞0.05).2组SpO2呈逐步上升的趋势,时点间差异有统计学意义(P＜0.05),组间、组间·时点间交互作用差异无统计学意义(P＞0.05).试验组术中丙泊酚用量少于对照组,苏醒时间短于对照组(P＜0.05).试验组术后5 min和30 min子宫收缩疼痛评分显著低于对照组,满意度优于对照组(P＜0.05).2组并发症发生率差异无统计学意义(P＞0.05).结论 盐酸纳布啡复合丙泊酚实施无痛人工流产术是一种安全有效的麻醉方法,可减少丙泊酚的用量,对术后子宫收缩疼痛有良好的镇痛效果,且未见明显不良反应.

KCNQ2/3 channels play an important role in controlling neuronal excitability. Agents that decrease KCNQ2/3 current amplitudes are proconvulsant, whereas KCNQ2/3 current enhancers are anticonvulsant. Levobupivacaine is able to block the KCNQ2/3 channels and enhance neuronal excitation, whereas retigabine is able to reopen the channels and thus reduce overexcitation of neurons. In this study, we aimed to determine if retigabine is able to abolish local-anesthetic-induced seizures.