BACKGROUND: Sevoflurane is widely used to anesthetize children because of its rapid action with minimal irritation of the airways. However, there is a high risk of agitation after emergence from anesthesia. Strabismus surgery, in particular, can trigger agitation because patients have their eyes covered in the postoperative period. The aim of this study was to determine whether or not esmolol and lidocaine could decrease emergence agitation in children. METHODS: Eighty-four patients aged 3 to 9 years undergoing strabismus surgery were randomly assigned to a control group (saline only), a group that received intravenous lidocaine 1.5 mg/kg, and a group that received intravenous esmolol 0.5 mg/kg and lidocaine 1.5 mg/kg. Agitation was measured using the objective pain score, Cole 5-point score, and Richmond Agitation Sedation Scale score at the end of surgery, on arrival in the recovery room, and 10 and 30 min after arrival. RESULTS: The group that received the combination of esmolol and lidocaine showed lower OPS and RASS scores than the other two groups when patients awoke from anesthesia (OPS = 0 (0-4), RASS = -4 [(-5)-1]) and were transferred to the recovery room (OPS = 0 (0-8), RASS = -1 [(-5)-3]) (P < 0.05). There was no significant difference in the severity of agitation among the three groups at other time points (P > 0.05). CONCLUSIONS: When pediatric strabismus surgery is accompanied by sevoflurane anesthesia, an intravenous injection of esmolol and lidocaine could alleviate agitation until arrival in the recovery room. TRIAL REGISTRATION Clinical Research Information Service, No. KCT0002925; https://cris.nih.go.kr/cris/en/search/search_result_st01.jsp?seq=11532.
Anesthesia ; methods ; Child ; Child, Preschool ; Double-Blind Method ; Humans ; Injections, Intravenous ; Lidocaine ; administration & dosage ; pharmacology ; Propanolamines ; administration & dosage ; pharmacology ; Sevoflurane ; therapeutic use ; Strabismus ; surgery ; Wakefulness ; drug effects

OBJECTIVETo investigate the effects of lidocaine on apoptosis and proliferation of hyperoxia-exposed type Ⅱalveolar epithelial cells (AECⅡ) from premature rats.

METHODSPrimary cultured AEC Ⅱ isolated from premature rats were randomly divided into four groups: air, air+ lidocaine (20 μg/mL), 95%O2/5%CO2, and 95%O2/5%CO2+ lidocaine. The cells in each group were collected 24 hrs after culture in ordinary incubators (37℃,5%CO2). The proliferation and apoptosis of AEC Ⅱ were detected by flow cytometry. Protein levels of proliferating cell nuclear antigen (PCNA) were measured by Western blot.

RESULTSThe apoptosis rate of AECⅡincreased, the percentages of G2/M and S phase cells decreased and the protein levels of PCNA decreased significantly in the group exposed to 95%O2/5%CO2 compared with the group exposed to air (P<0.01). Lidocaine treatment decreased apoptosis rate of AECⅡ, increased percentage of G2/M and S phase cells, and increased protein levels of PCNA.

CONCLUSIONSHyperoxia can increase apoptosis and inhibit proliferation of AECⅡ in premature rats. Lidocaine may have protective effects against the AECⅡ injuries.

Animals ; Apoptosis ; Cell Cycle ; Cytoprotection ; Epithelial Cells ; drug effects ; pathology ; Female ; Hyperoxia ; pathology ; Lidocaine ; pharmacology ; Male ; Proliferating Cell Nuclear Antigen ; analysis ; Pulmonary Alveoli ; drug effects ; pathology ; Rats ; Rats, Sprague-Dawley

This study is to investigate the effects of phenytoin sodium, lidocaine (sodium channel blockers), propranolol (beta-adrenergic receptor antagonist), amiodarone (drugs prolonging the action potential duration) and verapamil (calcium channel blockers) on arrhythmia of mice induced by Bufonis Venenum (Chansu) and isolated mouse hearts lethal dose of Chansu. Arrhythmia of mice were induced by Chansu and then electrocardiograms (ECGs) were recorded. The changes of P-R interval, QRS complex, Q-T interval, T wave amplitude, heart rate (HR) were observed. Moreover, arrhythmia rate, survival rate and arrhythmia score were counted. Isolated mouse hearts were prefused, and the lethal dose of Chansu was recorded. Compared with control group, after pretreatment with phenytoin sodium, broadening of QRS complex and HR were inhibited, and the incidence of ventricular arrhythmia was reduced dramatically, while survival rate was improved; the isolated mouse hearts lethal dose of Chansu was increased significantly. After pretreatment with lidocaine, the prolongation of P-R interval and broadening of QRS complex were inhibited, and the incidences of ventricular arrhythmia were reduced dramatically, while survival rate was improved; the isolated mouse hearts lethal dose of Chansu was increased significantly. After pretreatment with propranolol, prolongation of P-R interval, broadening of QRS complex, prolongation of Q-T interval and HR were inhibited, and the incidences of both supraventricular and ventricular arrhythmias were reduced dramatically, while survival rate was improved. After pretreatment with amiodarone, HR was inhibited, the incidences of ventricular tachycardia were reduced dramatically. Lastly, after pretreatment with verapamil, the prolongation of P-R interval and Q-T interval were inhibited and the incidences of both supraventricular and ventricular arrhythmias were reduced dramatically; the isolated mouse hearts lethal dose of Chansu was reduced significantly. In in vivo experiments, phenytoin sodium was most effective against the mice arrhythmias induced by Chansu while cautious use of verapamil for Chansu inducing arrhythmia should be noted. It is also concluded that mice ventricular arrhythmias induced by Chansu might be most closely related to sodium channel, supraventricular arrhythmias might be related to beta-adrenergic receptor, and calcium channel plays an important role in conduction block. In in vitro experiments, phenytoin sodium was most effective, followed by lidocaine and propranolol, and amiodarone had no obvious effect and verapamil reduced the lethal dose of Chansu.
Amiodarone ; pharmacology ; Animals ; Anti-Arrhythmia Agents ; pharmacology ; Arrhythmias, Cardiac ; chemically induced ; physiopathology ; Bufanolides ; toxicity ; Electrocardiography ; drug effects ; Female ; Heart Rate ; drug effects ; In Vitro Techniques ; Lethal Dose 50 ; Lidocaine ; pharmacology ; Male ; Mice ; Phenytoin ; pharmacology ; Propranolol ; pharmacology ; Verapamil ; pharmacology

OBJECTIVETo compare the effects of epidural anesthesia with 1.5% lidocaine and 0.5% ropivacaine on propofol requirements, the time to loss of consciousness (LOC), effect-site propofol concentrations, and the hemodynamic variables during induction of general anesthesia guided by bispectral index (BIS) were studied.

METHODSForty-five patients were divided into three groups to receive epidurally administered saline (Group S), 1.5% (w/w) lidocaine (Group L), or 0.5% (w/w) ropivacaine (Group R). Propofol infusion was started to produce blood concentration of 4 mug/ml. Once the BIS value reached 40~50, endotracheal intubation was facilitated by 0.1 mg/kg vecuronium. Measurements included the time to LOC, effect-site propofol concentrations, total propofol dose, mean arterial blood pressure (MABP), and heart rate (HR) at different study time points.

RESULTSDuring induction of anesthesia, both Groups L and R were similar for the time to LOC, effect-site propofol concentrations, total propofol dose, MABP, HR, and BIS. The total doses of propofol administered until 1 min post-intubation were significantly less in patients of Groups R and L compared with Group S. MABP and HR were significantly lower following propofol induction compared with baseline values in the three groups, or MABP was significantly increased following intubation as compared with that prior to intubation in Group S but not in Groups R and L while HR was significantly increased following intubation in the three groups.

CONCLUSIONEpidural anesthesia with 1.5% lidocaine and 0.5% ropivacaine has similar effects on the time to LOC, effect-site propofol concentrations, total propofol dose, and the hemodynamic variables during induction of general anesthesia.

Adult ; Amides ; pharmacology ; Anesthesia, Epidural ; Anesthesia, General ; Anesthetics, Local ; pharmacology ; Blood Pressure ; drug effects ; Electroencephalography ; Female ; Heart Rate ; drug effects ; Humans ; Lidocaine ; pharmacology ; Male ; Middle Aged ; Propofol ; pharmacology ; Time Factors

OBJECTIVETo study the protective effect of lidocaine against lung injury after hemorrhagic shock in rabbits.

METHODSEighteen healthy rabbits were randomly divided into 3 groups (n=6), namely lidocaine group (group L), hemorrhagic shock group (group H) and control group (group C). Hemorrhagic shock model was established in rabbits in groups L and H, and the venous blood samples were collected for measurement of plasma malondialdehyde (MDA) and superoxidedismutase (SOD) before phlebotomy (T0), 2 h after hemorrhagic shock (T1) and 2 h after resuscitation (T2). Blood samples were also taken for measurement of MDA and SOD at the same time points in group C. The wet to dry weight ratio of the lung (W/D) was measured at T2.

RESULTSMDA level was significantly lower while SOD level significantly higher in group L than in group H (P<0.05). The W/D ratio in group L was reduced significantly as compared with that in group H (P<0.05).

CONCLUSIONLidocaine can remarkably alleviate lung injury after hemorrhagic shock by inhibiting MDA production and increasing SOD content.

Animals ; Disease Models, Animal ; Lidocaine ; pharmacology ; Lung ; drug effects ; metabolism ; Lung Injury ; prevention & control ; Malondialdehyde ; blood ; Rabbits ; Shock, Hemorrhagic ; drug therapy ; Superoxide Dismutase ; blood

Animals ; Blood Pressure ; drug effects ; Electric Stimulation ; Female ; Habenula ; physiology ; Lidocaine ; pharmacology ; Male ; Raphe Nuclei ; physiology ; Rats ; Rats, Wistar ; Respiration ; drug effects ; Serotonin ; physiology

OBJECTIVE: To investigate the effect and possible mechanism of lidocaine precondition on calcium overload and apoptosis of the hepatocytes induced by cell hypoxia-reoxygenation. METHODS: The cultured L02 hepatocytes were randomly divided into 3 groups: a hypoxia-reoxygenation group (Group I), a lidocaine precondition group (Group II), and a normal control group (Group III). After 4 hours of cell hypoxia and 10 hours of reoxygenation, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations in the nutritive medium were detected. The cytoplasm ionic calcium concentration was measured by fluoro spectrophotometer. The apoptosis was measured by flow cytometry and fluorescent microscope. The appearance and ultra-microstructure changes of hepatocytes were observed by inverted microscope and electronic microscope. RESULTS: Cytoplasm ionic calcium concentration and apoptosis was positively correlated (r=0.7652, R(2)=0.5855, P< 0.05). The ALT concentration in the nutritive medium, AST concentration in the nutritive medium, cytoplasm ionic calcium concentration and the ratio of apoptosis of Group I and II were significantly higher than those of Group III(P< 0.05).The appearance and ultra-microstructure changes of Group I and II were worse than those of Group III. The ALT concentration in the nutritive medium, AST concentration in the nutritive medium, cytoplasm ionic calcium concentration and the ratio of apoptosis of Group II were significantly lower than those of Group I (P< 0.05). The ultra-microstructure injury of hepatocytes of Group II were less serious than those of Group I. CONCLUSION Precondition with lidocaine can attenuate calcium overload of hepatocytes induced by hypoxia-reoxygenation in vitro,and decrease the ratio of apoptosis.
Apoptosis ; drug effects ; Calcium ; metabolism ; Cell Hypoxia ; drug effects ; Cells, Cultured ; Hepatocytes ; cytology ; drug effects ; metabolism ; Humans ; Lidocaine ; pharmacology ; Oxygen ; metabolism

OBJECTIVE: To investigate the effect of lidocaine on LPS induced apoptosis of cultured adult rat alveolar Type II (AT-II) cells. METHODS: Cultured cells were exposed to LPS and lidocaine for 24 hours. Apoptosis and necrosis rates of cells were detected by flow cytometry and electron microscope. The activity of lactic dehydrogenase (LDH) was analyzed by using LDH kits. RESULTS: LPS induced the AT-II cell injuries by increasing not only the necrosis and apoptosis rates but also the LDH release of cultured AT-II in vitro. Lidocaine decreased the necrosis and apoptosis rates of AT-II cells. CONCLUSION Lidocaine can directly inhibit the apoptosis and necrosis induced by LPS in cultured AT-II cells.
Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Epithelial Cells ; pathology ; Flow Cytometry ; Lactate Dehydrogenases ; metabolism ; Lidocaine ; pharmacology ; Lipopolysaccharides ; Necrosis ; Protective Agents ; pharmacology ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Sprague-Dawley

AIMTo observe the effects of lidocaine and thiopental on the neuronal injury induced by the experimental ischemia in hippocampus slice cultures obtained from postnatal 22 days SD rats.

METHODSModel of the experimental ischemia was produced by hypoxia and glucose deprivation. Propidium iodide (PI) assay was used to observe the neuronal injury in CA1 and dentate gyrus (DG).

RESULTSAfter experimental ischemia, the peak of PI index was appeared in CA1 and DG on the first day (P < 0.01), PI index in DG was less than in CA1 (P < 0.01). PI indices were still higher during seven days after the experimental ischemia than before the experimental ischemia (P < 0.01). 10 nmol/L and 100 nmol/L concentration of lidocaine could significantly decrease PI indices in CA1 and DG (P < 0.01). 250 nmol/L and 600 nmol/L concentration of thiopental also decreased the PI indices in CA1 and DG (P < 0.01). The neuronal injury peaks were postponed to the third day after the experimental ischemia by lidocaine and thiopental.

CONCLUSIONIt suggested that lidocaine and thiopental could decrease the neuronal injury in CA1 and DG induced by the experimental ischemia, and postpone the neuronal injury peaks to the third day after the experimental ischemia.

Animals ; Brain Ischemia ; pathology ; CA1 Region, Hippocampal ; drug effects ; pathology ; In Vitro Techniques ; Lidocaine ; pharmacology ; Neurons ; drug effects ; pathology ; Rats ; Thiopental ; pharmacology

AIMTo study the cutaneous permeation kinetics and pharmacodynamics of lidocaine gel.

METHODSThe concentration of lidocaine in dermis following topical application in rats was determined by the cutaneous microdialysis technique and related parameters were calculated; the pharmacodynamics of the gel was evaluated by electric stimulation method with EMLA (eutectic mixture of local anesthetics) cream as a control.

RESULTSThe peak of percutaneous absorption kinetic profile of lidocaine gel across rat skin occurred at 1.25 h; the onset time of local anesthetic action of lidociane gel was similar to that of EMLA, but both the duration and depth of anesthetic effect were superior to EMLA cream.

CONCLUSIONLidocaine gel showed good anesthetic effect. The minimum effective concentration of lidocaine in dermis is 12 mg.L-1.

Anesthesia, Local ; Anesthetics, Local ; pharmacokinetics ; pharmacology ; Animals ; Gels ; Lidocaine ; pharmacokinetics ; pharmacology ; Male ; Pain Threshold ; drug effects ; Prilocaine ; pharmacokinetics ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar ; Skin Absorption