Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIDOCAINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1981

Blood concentration of lidocaine after spinal anaesthesia using lidocaine and lidocaine with adrenaline.

In 32 patients undergoing spinal anaesthesia with lidocaine or lidocaine plus adrenaline, the concentration of lidocaine base was measured in repeated venous blood samples. Half of the patients were given 100 mg lidocaine alone and the other half 100 mg lidocaine with the addition of 0.2 mg adrenaline. The blood concentration of lidocaine was significantly higher in the lidocaine group than in the group that received lidocaine with adrenaline. The mean maximal concentrations in these two groups lay between 0.2 and 0.3 and between 0.1 and 0.2 micrograms/ml, respectively (P less than 0.01). The time required for the individual maximal concentration to be reached was independent of whether the anaesthetic contained adrenaline or not. The blood concentration showed no correlation to body weight, height, or body surface area. In the first 60 min after the spinal injection the extent of the sensory block was the same in the two groups, but at 120 min this extent was significantly greater in the lidocaine-adrenaline group (P less than 0.01). The results show that the blood concentration of lidocaine is low in spinal anaesthesia compared with other types of regional anaesthesia.

Aged↗
PubMed1985

Serum concentrations and urinary excretion of lidocaine and its two desethylated metabolites after spinal anaesthesia using lidocaine or lidocaine with phenylephrine.

In 13 patients undergoing transurethral prostatic resection under spinal anaesthesia with heavy lidocaine or with heavy lidocaine plus phenylephrine hydrochloride, the serum concentrations of lidocaine, monoethylglycinexylidide and glycinexylidide and their renal excretion were measured with a HPLC method. Seven patients were given lidocaine alone 1.25 mg/kg and six lidocaine 1.25 mg/kg mixed with phenylephrine hydrochloride 3 mg. There was no significant difference between the two groups either in the serum levels of lidocaine or in the renal excretion rate of lidocaine and its metabolites. This finding gives support to the opinion that phenylephrine in low doses has no prolonging effect on spinal anaesthesia performed with heavy lidocaine.

Aged↗
PubMed1990

Comparison of lidocaine CO2, two per cent lidocaine hydrochloride and pH adjusted lidocaine hydrochloride for caesarean section anesthesia.

Lidocaine can be prepared in a variety of ways which may affect the characteristics of neural blockade achieved. Experimental evidence is equivocal as to the clinical impact of the use of different lidocaine preparations. A randomized, double-blind study was performed to investigate the differences in epidural anaesthesia for Caesarean section using three different lidocaine solutions: lidocaine CO2, two per cent lidocaine and two per cent lidocaine with its pH adjusted by the addition of bicarbonate. No differences were found among the groups in time of onset of neural blockade, quality or duration of neural blockade, time to delivery of the infant or volume of anaesthetic solution injected into the epidural space. A significant difference was found between the pH's of the solutions used. It is concluded that all three solutions are equally efficacious in epidural anaesthesia for Caesarean section.

Adult↗
PubMed2002

Comparison of effects of lidocaine hydrochloride, buffered lidocaine, diphenhydramine, and normal saline after intradermal injection.

STUDY OBJECTIVE: To evaluate pain and the spread of analgesia when local anesthetics are given as an intradermal injection into the dorsal aspect of the hand. DESIGN: Randomized, double-blinded, placebo-controlled study. SETTING: University medical center. PATIENTS: 40 consenting adult volunteers. INTERVENTIONS: Volunteers were randomly assigned to receive a 0.25-mL injection of either lidocaine hydrochloride (1%), buffered lidocaine, diphenhydramine (1%), or placebo (0.9% sodium chloride solution) into the dorsal aspect of both hands. MEASUREMENTS: The volunteers used a visual analog scale to compare the pain of needle insertion and solution injection. Then at 1, 2, 5, 10, 20, and 30 minutes after intradermal injection, the extent of the analgesic area was marked on a strip of tape placed horizontally across the hand. Then at 32 minutes after intradermal injection, the extent of the analgesic area was marked on a strip of tape placed vertically across the hand. The volunteers were called each day and asked the duration of their numbness or hyperesthesia until their hands were no longer numb or sore. MAIN RESULTS: Buffered lidocaine during intradermal infiltration was found to be significantly (p < 0.05) less painful than either lidocaine hydrochloride or diphenhydramine and equivalent to placebo. Diphenhydramine and lidocaine hydrochloride during intradermal infiltration induced significantly (p < 0.05) more pain than buffered lidocaine or placebo. Lidocaine hydrochloride displayed a significantly (p < 0.05) larger diameter of analgesia than placebo by 1 minute after the injection, buffered lidocaine by 2 minutes after injection, and diphenhydramine by 5 minutes after injection. By 20 minutes after injection, diphenhydramine diameter of analgesia was significantly (p < 0.05) larger than placebo but significantly less than buffered lidocaine. By 30 minutes after injection, diphenhydramine diameter of analgesia was equivalent to placebo whereas buffered lidocaine and lidocaine diameters were still significantly (p < 0.05) larger than placebo. Diphenhydramine injection resulted in numbness that lasted significantly (p < 0.05) longer than other study solutions whereas buffered lidocaine and lidocaine injections resulted in numbness that lasted significantly longer than placebo. Diphenhydramine injection resulted in hyperesthesia that lasted for 2 or more days in 12 of the volunteers. CONCLUSION: There is a reduction of infiltration pain using buffered lidocaine as opposed to lidocaine and diphenhydramine. Although lidocaine injection resulted in a slightly faster spread of analgesic diameter, buffered lidocaine was equivalent to lidocaine from minute 2 until minute 30. Therefore, to obtain optimal anesthetic conditions, we recommend that buffered lidocaine be given 2 minutes before performing catheterization, whereas diphenhydramine should be given 5 minutes before catheterization, but only when buffered lidocaine cannot be used.

Adult↗
PubMed2000

Concentrations of lidocaine and monoethylglycine xylidide in brain, cerebrospinal fluid, and plasma during lidocaine-induced epileptiform electroencephalogram activity in rabbits: the effects of epinephrine and hypocapnia.

UNLABELLED: When injecting lidocaine into tissues, the mean toxic dose of lidocaine may be increased by adding epinephrine to lidocaine and by decreasing the PaCO(2). In contrast, when lidocaine is introduced directly into an artery or vein, adding epinephrine to lidocaine may decrease the mean toxic dose of lidocaine. Less is known about the effects of decreased PaCO(2) on intravascular lidocaine toxicity. We infused lidocaine in 24 rabbits at 4 mg. kg(-1). min(-1) with/without epinephrine and with/without hypocapnia. We measured the time to onset of lidocaine-induced seizures, total dose of lidocaine at the time of seizures, and concentrations of lidocaine and monoethylglycine xylidide (MEGX), a metabolite of lidocaine, in plasma, brain, and cerebrospinal fluid. Epinephrine decreased onset time by 11% with hypocapnia and by 21% with normocapnia, and it increased plasma MEGX by 1 microg/mL with hypocapnia and 2 microg/mL with normocapnia. Hypocapnia increased onset time by 18% without epinephrine and by 33% with epinephrine, and it increased whole-brain MEGX by 10 microg/mL without epinephrine and by 14 microg/mL with epinephrine. We conclude that, when lidocaine is given intravascularly, hypocapnia increases onset time and lidocaine dose required for seizures. These effects occur with no change in the concentration of lidocaine in plasma or the brain. IMPLICATIONS: Hypocapnia increases the toxic dose of lidocaine given IV without altering lidocaine concentrations in blood, brain, or cerebrospinal fluid. Whole-brain monoethylglycine xylidide concentration is greater during hypocapnia than during normocapnia, and the addition of epinephrine to lidocaine increases the concentration of monoethylglycine xylidide in plasma.

Anesthetics, Local↗
PubMed1999

Topical lidocaine-prilocaine versus lidocaine for neonatal circumcision: a randomized controlled trial.

OBJECTIVE: To evaluate epicutaneous application of 5% lidocaine-prilocaine and 30% lidocaine cream anesthetics for neonatal circumcision. METHODS: The efficacy of 5% lidocaine-prilocaine and 30% lidocaine creams was compared in a randomized, double-blind, placebo-controlled trial. Sixty-one neonates were randomly assigned to one of three groups: 5% prilocaine-lidocaine (n = 20), 30% lidocaine (n = 20), and a control group that received an acid-mantle cream (n = 21). Heart rate, oxygen saturation, and crying time were monitored before, during, and after circumcision. Blood pressure was measured before and after circumcision. RESULTS: Mean peak heart rates for the 5% lidocaine-prilocaine, 30% lidocaine, and control groups (+/- standard deviation) were 146 +/- 16, 157 +/- 10, and 164 +/- 16 beats per minute, respectively. During four of six active phases of circumcision, the 5% lidocaine-prilocaine group suppressed significant increases in heart rate better than 30% lidocaine, which was more effective than control (dorsal clamp, P < .001; bell clamp on, P = .001; tightening, P = .001; bell clamp off, P < .001). During tightening of the bell clamp, significantly less crying was seen in the 5% lidocaine-prilocaine group (13 +/- 12 seconds) compared with 30% lidocaine (24 +/- 14 seconds) and controls (38 +/- 27 seconds) (P < .001). The group that received 5% lidocaine-prilocaine also had no significant increase in systolic (t = 1.6, P = .12) or diastolic (t = 1.9, P = .067, respectively) blood pressure, unlike the group receiving 30% lidocaine (t = 4.8, P = .001 and t = 2.9, P = .009, respectively) and the placebo group (t = 2.5, P = .023 and t = 2.3, P = .032). There were no significant differences in oxygen saturation (alpha = .05, power 0.79). CONCLUSION: Epicutaneous 5% lidocaine-prilocaine was more effective than 30% lidocaine for neonatal circumcision, better reducing neonatal stress indicators. Lidocaine-prilocaine significantly shortened crying time during one of the most painful phases of circumcision. Both topical anesthetics were more effective than placebo in attenuating the behavioral and physiologic indicators of neonatal pain.

Anesthesia, Local↗
PubMed1996

Prevention of lidocaine aerosol-induced bronchoconstriction with intravenous lidocaine.

BACKGROUND: Lidocaine applied topically provokes bronchoconstriction in persons with hyperreactive airway disease. The authors questioned whether intravenous lidocaine would prevent lidocaine-aerosol induced bronchoconstriction. They compared the effects of lidocaine administered intravenously and by the aerosol route on baseline airway tone, and on the prevention of histamine-induced bronchoconstriction in five Basenji-Greyhound dogs. METHODS: Dogs were pretreated with either intravenous or aerosol lidocaine followed by histamine aerosol challenge. On separate days, dogs were pretreated with intravenous lidocaine, followed by aerosol lidocaine administration at similar doses. Airway caliber was assessed using high-resolution computed tomography. Data were analyzed by two-way analysis of variance. Serum lidocaine concentrations were obtained. RESULTS: Histamine alone decreased the airway area by 32 +/- 3%. Lidocaine administered intravenously or by the aerosol route significantly inhibited histamine-induced bronchoconstriction. There was no significant difference between the two routes in preventing histamine-induced bronchoconstriction. At the dose that inhibited histamine-induced bronchoconstriction, lidocaine administered by the aerosol route decreased baseline airway area by 27 +/- 3% (P < 0.01), whereas intravenous lidocaine had no effect. Intravenous lidocaine prevented lidocaine aerosol-induced bronchoconstriction, and the combination of intravenous and aerosol lidocaine significantly dilated the airways by 20 +/- 5% (P < 0.01 compared with control). CONCLUSIONS: An intravenous bolus of lidocaine prevents the initial bronchoconstriction induced by lidocaine when administered as an aerosol.

Aerosols↗
PubMed1986

Effect of duration of lidocaine infusion and route of cimetidine administration on lidocaine pharmacokinetics.

The effects of the duration of lidocaine infusion and the route of cimetidine administration on lidocaine pharmacokinetics were evaluated in a randomized, three-phase crossover study of six healthy men. Lidocaine hydrochloride 100 mg was administered intravenously over two minutes, and plasma lidocaine concentrations were determined before treatment and at various intervals for three hours. Immediately after the three-hour sample was obtained, a second 100-mg dose of lidocaine hydrochloride was given, followed by a 21-hour constant infusion at a rate of 2 mg/min. Plasma lidocaine concentrations were determined at various intervals during the infusion and for eight hours afterward. Urine was collected during the last five hours of the infusion and assayed for lidocaine, monoethylglycinexylidide (MEGX), and glycinexylidide (GX). The following treatments were administered to each subject in a crossover manner: a placebo tablet every six hours, beginning two days before lidocaine administration; cimetidine 300 mg orally every six hours, beginning two days before lidocaine administration; and cimetidine hydrochloride 300 mg i.v. every six hours, beginning one hour before lidocaine administration. Each medication was given until the lidocaine infusion was discontinued. Subjects fasted and remained supine throughout each treatment period. Oral cimetidine increased the area under the concentration-time curve for lidocaine by 14.7% and increased the elimination half-life of lidocaine; i.v. cimetidine did not have a significant effect on lidocaine disposition. Lidocaine clearance was 34% lower under steady-state than single-dose conditions, but the effects of cimetidine on lidocaine disposition were similar under both conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Therapeutic serum lidocaine and metabolite concentrations in patients undergoing electrophysiologic study after discontinuation of intravenous lidocaine infusion.

Serum concentrations of lidocaine and its metabolites monoethylglycinexylidide (MEGX) and glycinexylidide (GX) were measured in seven patients after discontinuation of intravenous lidocaine necessary for control of spontaneous arrhythmias prior to electrophysiologic study. Standard loading doses of lidocaine were given intravenously followed by 2 mg/min infusions for 79.5 +/- 6.5 hours. Electrophysiologic studies all started more than 5 half-lives or 7.5 hours after discontinuation of intravenous lidocaine. Local anesthesia with subcutaneous lidocaine (mean 162 +/- 96 mg) was administered in six patients. Plasma concentrations of lidocaine and its metabolites were determined at the termination of the infusion, 2 and 4 hours afterwards, at the start of the electrophysiologic study prior to local anesthesia, and at the end of the study. Levels were also determined at 12 and 24 hours after discontinuation of the infusion. Mean plasma concentrations of lidocaine, MEGX, and GX at the start of the study were 1.02, 0.86, and 0.62 micrograms/ml, respectively. These had increased to 2.78, 0.92, and 0.68 by the end of the electrophysiologic study. One patient with coronary artery disease and prior out-of-hospital ventricular fibrillation had a therapeutic lidocaine level and no inducible arrhythmia at the time of the initial study. At a subsequent electrophysiologic study, no lidocaine or metabolites were detected in the serum and ventricular fibrillation was induced. Thus using the reported half-life of 90 minutes and discontinuing lidocaine 5 half-lives prior to electrophysiologic evaluation does not ensure lack of electrophysiologic effects of the parent compound or its metabolites. Lidocaine given for local anesthesia further increases lidocaine and metabolite levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1996

Cocaine concentration-effect relationship in the presence and absence of lidocaine: evidence of competitive binding between cocaine and lidocaine.

UNLABELLED: To better understand the interaction between cocaine and lidocaine, we studied the cocaine's concentration-effect relationship for action potential duration (APD) and the rate of rise of phase 0 of the action potential (Vmax) of canine papillary muscle in the presence and absence of lidocaine. We measured APD and Vmax during programmed stimulation and superfusion with normal Tyrode's, 30 microM cocaine and 30 microM cocaine + 30 microM lidocaine. Using two microelectrodes, we simultaneously recorded action potentials from two sites during programmed stimulation and measured the conduction velocity and effective refractory period during exposure to normal Tyrode's, cocaine and cocaine + lidocaine. Cocaine with or without lidocaine delayed the plateau of the APD restitution curve. At 1000 msec cycle length, the addition of 30 microM lidocaine to the superfusate containing 30 microM cocaine shortened the time constant for reactivation of Vmax from 514 +/- 63 to 234 +/- 28 msec (P < .01). Lidocaine also improved the conduction velocity decreased by cocaine, but did not significantly change the effective refractory period. The configuration of cocaine concentration-effect curve for APD was biphasic. For cocaine concentrations < 100 microM, APD progressively shortened prolonged with increasing concentrations. As cocaine concentrations increased > 100 microM, APD progressively shortened. The addition of lidocaine to the superfusate with cocaine > 100 microM tended to attenuate the progressive APD shortening due to cocaine. Lidocaine shifted the curve correlating cocaine concentration and reduction of Vmax rightward, but preserved Emax at cocaine concentration > 225 microM. These findings suggest competitive antagonism between cocaine and lidocaine at a single sodium channel receptor. CONCLUSION: lidocaine displaces cocaine from the sodium channel receptor through competitive binding. Lidocaine may prove to be beneficial in reversing cocaine-induced slowing of ventricular conduction.

Action Potentials↗
PubMed2003

Lidocaine 2% gel versus lidocaine 4% unpreserved drops for topical anesthesia in cataract surgery: a randomized controlled trial.

OBJECTIVE: To compare intracameral levels and clinical efficacy of lidocaine 2% gel with lidocaine 4% unpreserved drops. DESIGN: Double-blind, randomized, one-surgeon, controlled trial. PARTICIPANTS: One hundred seven consecutive cataract cases eligible for topical anesthesia. INTERVENTION: Patients were randomly assigned to receive 20 mg of lidocaine either as lidocaine 2% gel (1 ml) or as lidocaine 4% unpreserved eyedrops (0.5 ml) before clear corneal phacoemulsification. MAIN OUTCOME MEASURES: Aqueous samples were taken to measure lidocaine intraocular levels. Intraoperative pain was quantified a few minutes after surgery using a 0 to 10 visual analog scale. SECONDARY OUTCOME MEASURES: Patients were asked to grade the degree to which they were bothered by tissue manipulation. The surgeon graded patients' cooperation. The anesthesiologist recorded any increase in pulse or blood pressure and the need for supplemental topical anesthesia or intravenous sedation. Duration of surgery and intraoperative complications were also recorded. RESULTS: In the gel group intracameral lidocaine levels were significantly higher (P < 0.001) and patient-reported intraoperative pain scores were significantly lower (P = 0.026). Patients in the gel group were bothered by tissue manipulation to a lesser extent (P = 0.028), and their cooperation was better (P = 0.002). Increases in blood pressure were more frequent in the eyedrops group. Supplemental anesthesia was required in two cases (3.70%) in the gel group versus eight cases in the eyedrops group (15.09%). No correlation between intracameral lidocaine levels and intraoperative pain scores was found (r = -0.026, P = 0.789). CONCLUSIONS: If administered by means of gel, the same amount of lidocaine gives significantly higher intracameral levels of lidocaine, better analgesia, better patient cooperation, and less need for intraoperative supplemental anesthesia. Lower pain scores do not correlate with intracameral lidocaine levels.

Aged↗
PubMed2002

Lidocaine toxicity during frequent viscous lidocaine use for painful tongue ulcer.

Oral viscous lidocaine is useful for the treatment of symptoms induced by oral inflamed mucosa, such as radiation- or chemotherapy-induced mucositis. The toxic reactions associated with an accidental overdose have been reported in pediatric cases. We report a case of lidocaine toxicity in a 22-year-old man during frequent viscous lidocaine use for severe painful tongue ulcer. The toxic symptoms developed when the amount of oral viscous lidocaine exceeded 240 ml per day. The serum lidocaine concentration associated with this use was 6.7 microg/ml. The toxic symptoms continued in spite of the serum lidocaine concentration below the toxic level after the start of a diluted preparation, which contained a half-dose lidocaine. It is speculated that lidocaine metabolites might have contributed to the toxic symptoms. Clinicians should consider the risk of lidocaine toxicity in cases of frequent viscous lidocaine use, and determine the serum concentrations of lidocaine and its metabolites.

Administration, Oral↗
PubMedDate not supplied

Plasma concentrations of lidocaine and its principal metabolites during continuous epidural infusion of lidocaine with or without epinephrine.

BACKGROUND AND OBJECTIVES: The purpose of this study was to evaluate the effect of epinephrine on the absorption of lidocaine and the accumulation of active metabolites of lidocaine during continuous epidural anesthesia. METHODS: Lidocaine was administered as an initial bolus of 5 mg/kg of 2% lidocaine solution followed by continuous infusion at 2.5 mg/kg/h. Patients in group I (n = 10) received lidocaine alone and patients in group II (n = 10) received lidocaine + epinephrine (5 pg/mL). Concentrations of lidocaine and its active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX), were measured in plasma samples obtained after 15 minutes, 30 minutes, and 1, 2, and 3 hours of infusion using high-performance liquid chromatography with ultraviolet detection. RESULTS: Plasma lidocaine concentrations were higher in group I for the first 30 minutes; however, after 1 hour the levels were the same. Plasma MEGX and GX increased continuously in both groups. MEGX levels the were significantly higher in group I, but there was no significant difference in the sum of lidocaine + MEGX after 2 hours. There was no significant difference in GX levels between the two groups. CONCLUSIONS: With respect to continuous epidural administration, addition of epinephrine to lidocaine solutions is ineffective after 2 hours for reducing the potential for systemic toxicity, because the sum of the plasma concentrations of lidocaine and its principal active metabolite, MEGX, are unaffected.

Absorption↗
PubMed1995

Effect of vasoconstrictive agents added to lidocaine on intravenous lidocaine-induced convulsions in rats.

BACKGROUND: Epinephrine is reported to decrease the threshold of intravenous lidocaine-induced convulsions. However, the mechanism underlying this effect is not clear. Therefore, we carried out a study to examine the role of vasopressor-induced hypertension. METHODS: Fifty-six awake Wistar rats were assigned to seven groups of eight. All groups received a continuous intravenous infusion of lidocaine at a rate of 4 mg.kg-1.min-1 until generalized convulsions occurred. The control group (group C) received plain lidocaine. The acute hypertensive groups received lidocaine with epinephrine (group E), norepinephrine (group N), or phenylephrine (group P) to increase mean arterial blood pressure (MAP) to 150 +/- 5 mmHg. Sodium nitroprusside (SNP) was added to prevent an increase in mean arterial pressure in the remaining three groups (vasopressor-SNP groups). RESULTS: The acute hypertensive groups required significantly smaller cumulative doses of lidocaine to produce convulsions compared with control (C = 41.5 +/- 2.9 > E = 24.1 +/- 2.7, N = 27.1 +/- 2.8, P = 26.7 +/- 2.5 mg.kg-1; values are mean +/- SD, P < 0.01). In addition, plasma lidocaine concentrations (C = 11.0 +/- 0.7 > E = 7.4 +/- 0.5, N = 7.9 +/- 0.6, P = 8.1 +/- 0.8 micrograms.ml-1, P < 0.01) and brain lidocaine concentrations (C = 50.9 +/- 4.5 > E = 32.6 +/- 4.2, N = 34.5 +/- 4.8, P = 37.1 +/- 4.5 micrograms.g-1, P < 0.01) were less in the acute hypertensive groups at the onset of convulsions. In the vasopressor-SNP groups, the plasma and brain lidocaine concentrations at the onset of convulsions returned to the control values, although epinephrine and norepinephrine, but not phenylephrine, still decreased cumulative convulsant doses of lidocaine significantly (P < 0.01) compared with control (E + SNP = 30.8 +/- 2.9 < N + SNP = 34.8 +/- 2.8, P < 0.01) < P + SNP = 40.2 +/- 3.0 mg.kg-1, P < 0.01). The brain/plasma concentration ratios were similar for the seven groups. CONCLUSIONS: An equal degree of acute hypertension induced by these three different vasopressors may play a role in reducing the threshold (plasma and brain lidocaine concentrations) as well as the cumulative convulsant doses associated with lidocaine-induced convulsions.

Acute Disease↗
PubMed1998

Combined intravenous lidocaine and inhaled salbutamol protect against bronchial hyperreactivity more effectively than lidocaine or salbutamol alone.

BACKGROUND: Airway instrumentation in persons with asthma is linked to the risk of life-threatening bronchospasm. To attenuate the response to airway irritation, intravenous lidocaine is recommended (based on animal experiments) and mitigates the response to histamine inhalation in asthmatic volunteers. However, the effects of lidocaine have not been compared with standard prophylaxis with beta-sympathomimetic aerosols. Therefore, the effect of lidocaine, salbutamol, combined treatment, and placebo control were tested in awake volunteers with bronchial hyperreactivity. METHODS: After approval from the local ethics committee, 15 persons, who were selected because they showed a decrease in forced expiratory volume in 1 s (FEV1) more than 20% of baseline in response to inhaled histamine in a concentration less than 18 mg/ml (PC20), were enrolled in a placebo-controlled, double-blind, and randomized study. The challenge was repeated on four different days and the volunteers were pretreated with either intravenous lidocaine, inhalation of salbutamol, inhalation of salbutamol plus intravenous lidocaine, or placebo. Lidocaine plasma concentrations were also measured. Statistical analyses included the Friedman test and Wilcoxon's rank sum. RESULTS: The baseline PC20 was 6.4 +/- 4.3 mg/ml. Intravenous lidocaine and salbutamol aerosol both significantly increased the histamine threshold to 14.2 +/- 9.5 mg/ml and 16.8 +/- 10.9 mg/ml, respectively (mean +/- SD). However, the combination of lidocaine and salbutamol significantly increased the PC20 even further to 30.7 +/- 15.7 mg/ml than did salbutamol or lidocaine alone. CONCLUSIONS: In volunteers with bronchial hyperreactivity, both lidocaine and salbutamol attenuate the response to an inhalational histamine challenge, and their combined administration has much greater effects than does either drug alone. Accordingly, pretreatment of patients with bronchial hyperreactivity with both beta-mimetic aerosol and intravenous lidocaine is recommended before airway irritation.

Administration, Inhalation↗
PubMed1988

Venous blood concentration of lidocaine after nasopharyngeal application of 2% lidocaine gel.

In 34 subjects undergoing topical anaesthesia with lidocaine gel (2% xylocaine gel), the concentrations of lidocaine base were measured in repeated venous blood samples. Twenty-three patients (Group I) were given 20 ml of 2% lidocaine gel (400 mg of lidocaine) and six subjects (Group II) 40 ml of 2% lidocaine gel (800 mg of lidocaine) nasopharyngeally, the gel reaching the pharynx being swallowed. Five minutes after administration of the gel, a gastric tube was introduced via the nasal cavity. In six patients (Group III), the bladder was catheterised in addition to insertion of a gastric tube. Before the catheter was introduced, these patients were given lidocaine gel nasopharyngeally (400 mg) and endourethrally (400 mg). After the introduction of the gastric tube, all subjects (except four volunteers in Group II) were given general anaesthesia. Before intubation, the patients in Group III also received lidocaine spray laryngotracheally (50 mg; 10% xylocaine spray). The initial absorption of lidocaine was rapid, although the blood concentrations were low. The mean peak concentrations (Cmax) of lidocaine in the three groups were 0.57, 1.39 and 0.73 micrograms/ml, respectively. The blood concentration in Group II was significantly higher than those in Groups I and III. The mean length of time between the nasopharyngeal application of lidocaine gel and the time when Cmax was reached (tpeak) was the same in all three groups (60-70 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMedDate not supplied

A comparison between lidocaine alone and lidocaine with meperidine for continuous spinal anesthesia.

BACKGROUND AND OBJECTIVES: Experimental investigations have demonstrated a synergistic interaction between opioids and local anesthetics. This study aims to assess the effective benefit-risk ratio of continuous spinal anesthesia (CSA) induced with either 1.6% lidocaine alone or in combination with 1% meperidine. METHODS: Thirty-four elderly patients (80.7 +/- 7.3 years) operated on for fracture of the neck of the femur were randomly allocated to two groups. In the first group (n = 15), CSA was induced with lidocaine 1.6% plain, whereas in the second group (n = 19) 1% meperidine was added. Reinjections were performed in both groups using lidocaine 1.6% alone. RESULTS: In the lidocaine group, 43 +/- 13 mg was used for induction whereas in the other group the addition of 18 +/- 5 mg of meperidine significantly reduced the dose of lidocaine required to 28 +/- 8 mg (p < 0.001). Delay between two reinjections was increased to 51 +/- 7 minutes in the lidocaine plus meperidine group, compared to 35 +/- 6 minutes in the lidocaine group (p < 0.001). Ephedrine was required for 9 out of the 19 patients in the lidocaine plus meperidine group, whereas it was required for only two patients in the other group (p = 0.05). Mean plasma concentrations of meperidine 1 hour and 3 hours after induction was 45.5 +/- 12 ng/ml and 59 +/- 22 ng/ml, respectively, and drowsiness was observed in 95% of the patients in the second group. Delay before requirement for pain medication was 2.2 +/- 2 hours in the lidocaine group and 14.1 +/- 8 hours in the lidocaine plus meperidine group (p < 0.001). CONCLUSIONS: The association of 1% meperidine with 1.6% lidocaine during the induction of CSA decreases the initial induction dose, prolongs analgesia, produces initial drowsiness, and provides long-lasting pain relief. However, such benefits are offset by some impairment of hemodynamic stability that is likely to make this combination of drugs unacceptable as an enhanced analgesic technique.

Aged↗
PubMed1977

Effect of lidocaine and methyl lidocaine on cardiac conduction.

The effects of lidocaine and methyl lidocaine on cardiac conduction were studied using His bundle recordings from isolated blood perfused dog hearts. The input and output characteristic of the atrioventricular (AV) node can be described as consisting of three components, namely, minimal conduction time, fatigue, and the effect of prematurity (deltaCT). Lidocaine (2.5-10.0 mg/kg) increased minimal conduction time but not fatigue. Methyl lidocaine (1.25-5.0 mg/kg) increased both. A dose of 5 mg/kg or less of either drug caused a nonparallel shift of the deltaCT curve to the right. High doses of lidocaine (10 mg/kg) cause deltaCT to become rate-dependent. Lidocaine slowed atrial conduction only slightly. Atrial block prevented the observation of the effect of methyl lidocaine in doses higher than 5.0 mg/kg. Both drugs showed greater effect on atrial conduction at fast heart rate. Lidocaine did not affect ventricular conduction time at slow heart rates and had only minimal effects at fast heart rates. Methyl lidocaine increased ventricular conduction time at all heart rates. The results of this study indicate that lidocaine and methyl lidocaine have entirely different spectra of activity on cardiac conduction, in that their effect on AV nodal conduction do not differ greatly whereas the quaternary analog has a much stronger depressant effect on atrial and ventricular conduction.

Animals↗