[Depressive effect of dibucaine and bupivacaine on the growth of axons from cultured neuron of Lymnaea stagnalis].

The depressive effect of dibucaine (n = 8) was compared with that of bupivacaine (n = 9) using identified cultured neurons (A cluster) of Lymnaea stagnalis. Cultured interneurons exhibit extensive neurite outgrowth within 14-20 hours when placed in brain conditioned media. The changes of cultured neuron were recorded using a color video camera directly connected to an inverted microscope and the images were stored on digital video tape. Local anesthetics were added to the culture dish, with final concentrations of 1 x 10(-6) M-8 x 10(-4) M of dibucaine and 1 x 10(-5) M-8 X 10(-3) M of bupivacaine. We examined the damage of growth cone before and 30 minute after local anesthetics administration. Histologic damage were scored from moderate to severe compared to the control before dibucaine or bupivacaine administration. Dibucaine or bupivacaine damaged the growth cone moderately in the concentration of 1 x 10(-5) M or 4 x 10(-4) M, respectively. While dibucaine or bupivacaine damaged it severely in the concentration of 8 x 10(-5) M or 2 x 10(-3) M, respectively. These results suggest that bupivacaine is safer than dibucaine with the concentration we use in clinical practice.

[Comparison of epidural anesthesia and general anesthesia for patients with bronchial asthma].

We prospectively investigated the incidence of asthmatic attacks in 94 patients (1.5%) who were diagnosed as definite asthma. We separated the patients into three groups: epidural anesthesia (n = 10) including combined spinal/epidural anesthesia (n = 7), combined epidural and general anesthesia (n = 23), and general anesthesia (n = 54). General anesthesia was induced with propofol or midazolam and maintained with N2O and O2 with sevoflurane in adults. Patients who underwent epidural anesthesia and combined spinal and epidural anesthesia showed no asthmatic attacks. The incidence of bronchospasm with combined epidural and general anesthesia was 2/23. The incidence of bronchospasm with general anesthesia was 4/54. Bronchoconstriction occurred after tracheal intubation in 5 patients except in one patient, in whom it occurred after induction of anesthesia with midazolam. All episodes of bronchospasm in the operative period were treated successfully. The frequency of bronchospasm did not depend on the severity of asthmatic symptoms or the chronic use of bronchodilators before operation. These findings suggest that tracheal intubation, not the choice of anesthetic, plays an important role in the pathogenesis of bronchospasm.

Ephedrine, dopamine, or dobutamine to treat hypotension with propofol during epidural anesthesia.

PURPOSE: To compare the efficacy of ephedrine, dopamine and dobutamine for circulatory support during thoracic epidural anesthesia after anesthetic induction with propofol. METHODS: Forty patients undergoing lobectomy or mastectomy were divided into four groups of 10: a control group received no vasopressor; an ephedrine group received 5 mg ephedrine when the mean arterial pressure (MAP), measured every 2.5 min, decreased by 10% from baseline; dopamine and dobutamine groups received 5 microg x kg(-1) x min(-1) dopamine or 3 microg x kg(-1) x min(-1) dobutamine from five minutes after epidural injection of local anesthetic to the end of tracheal intubation. Anesthesia was induced with 2 mg x kg(-1) propofol. The MAP and heart rate (HR) were measured at baseline, 20 min after epidural injection, three minutes after propofol, and one minute after tracheal intubation. RESULTS: In the control group, MAP and HR decreased from 86+/-9 mmHg, 74+/-8 bpm to 62+/-9 mm Hg; P<0.0001, 60+/-8 bpm; P = 0.0003 after propofol. After tracheal intubation, MAP was restored to (81+/-13 mmHg, 70+/-13 bpm). In the ephedrine, dopamine, and dobutamine groups, MAP and HR remained unchanged during epidural anesthesia and propofol induction. However, after tracheal intubation, MAP and HR increased in the ephedrine (104+/-11 mm Hg; P = 0.004, 87+/-11 bpm; P<0.0001) and dobutamine (117+/-13 mm Hg; P = 0.0005, 100+/-11 bpm; P<0.0001) groups, but not in the dopamine group compared with baseline. CONCLUSION: Dopamine is preferable to ephedrine and dobutamine in providing hemodynamic stability during propofol induction and tracheal intubation following epidural anesthesia.

[Analysis of inadvertent epidural injection of drugs].

We asked 31 anesthesiologists, who were on the Japanese Board of Anesthesiology, about inadvertent injection of drugs into the epidural space, and received answers from 28 (90%). Fifteen (54%) had an experience of inadvertent epidural injection, and five of them had two experiences. Injected drugs were ephedrine (6 times), a mixture of neostigmine and atropine (3), thiopental (2), etilefrine (2), vecuronium (1), suxamethonium (1), bicarbonate (1), midazolam (1), lactated Ringer's solution (1), nicardipine (1), and pentazocine (1). The inadvertent injection of thiopental or bicarbonate was noticed by back pain during injection. No treatment was added after the inadvertent injections, except a patient with an epidural steroid injection following thiopental. No neurological complications were found in any patients.

Effects of levobupivacaine, bupivacaine, and ropivacaine on tail-flick response and motor function in rats following epidural or intrathecal administration.

BACKGROUND AND OBJECTIVES: Commercially available bupivacaine is a racemic mixture of S (-)- and R(+)-enantiomers. Although the S(-)-enantiomers levobupivacaine and ropivacaine are less toxic to the cardiovascular and central nervous systems than bupivacaine, their relative efficacy has not been determined. This study directly compares the dose response of levobupivacaine, ropivacaine, and bupivacaine following epidural and intrathecal administration in the rat. METHODS: The time course of change in tail-flick latency and qualitative motor function was studied in rats following epidural or intrathecal administration of 0.25-0.75% levobupivacaine, ropivacaine, or bupivacaine in blinded, randomized fashion. RESULTS: Levobupivacaine and bupivacaine produced comparable and significantly enduring antinociceptive effects compared with ropivacaine at all test concentrations following both epidural and intrathecal administrations. Duration of motor block at lower local anesthetic concentrations (epidurally and intrathecally) was comparable with levobupivacaine and ropivacaine but significantly shorter than with bupivacaine. Epidural 0.75% levobupivacaine and bupivacaine showed more enduring motor block than ropivacaine. CONCLUSIONS: Levobupivacaine, given epidurally or intrathecally, produces longer lasting antinociceptive action than ropivacaine at equivalent concentrations and similar motor blocking effect at lower concentrations in both epidural and intrathecal administrations. Levobupivacaine-induced prolongation of the tail-flick latency is comparable to that of bupivacaine, as is motor blocking effect at higher concentrations. The possibility of significant differential block with levobupivacaine compared with bupivacaine warrants further study.

[Effect of epidural anesthesia on airway constriction induced with methacholine or capsaicin in cats].

The choice of epidural anesthesia for patients with bronchial asthma is controversial. We studied the effect of epidural anesthesia on airway constriction induced by methacholine or capsaicin in cats. Cats were anesthetized with pentobarbital and mechanically ventilated. Peak airway pressure and compliance, as well as cardiac sympathetic and vagal nerve activity were recorded. We sprayed 0.2% methacholine of 0.2% capsaicin into the trachea to produce airway constriction, and 15 min after drug spray we injected 2% lidocaine 1.0 ml into the epidural space. Methacholine increased peak airway pressure by 25% and decreased compliance by 26%. Capsaicin increased peak airway pressure 20% and decreased compliance 22%. After epidural anesthesia, cardiac sympathetic nerve activity decreased to 40% and 44%, vagal nerve activity decreased to 92% and 61% of control values in methacholine and capsaicin groups, respectively. However, here were no changes in the peak airway pressure and compliance in the two groups. These results suggest that epidural anesthesia, even if epidural anesthesia decrease sympathetic nerve activity, has no effect on the airway constriction induced with methacholine or capsaicin.

[The effects of flumazenil or bicuculline on the respiratory depression by morphine].

The effects of intravenous administration of flumazenil (n = 6) or bicuculline (n = 6) on the discharge of the phrenic nerve were studied following vagotomy in pentobarbital anesthetized mechanically ventilated rats. Morphine (0.4 mg.kg-1.min-1) was administrated until the respiratory rate decreased to about a half of the baseline respiratory rate. In this state, we first administered flumazenil (0.25 mg.kg-1) or bicuculline (0.4 mg.kg-1), intravenously and then administered naloxone (0.02 mg) intravenously in the two groups. The increase of inspiratory time from 0.7 +/- 0.1 to 2.0 +/- 0.5 s by morphine recovered to 0.8 +/- 0.2 s by bicuculline and to 0.6 +/- 0.1 s by naloxone. The increase of inspiratory time from 0.7 +/- 0.1 to 1.7 +/- 0.3 s by morphine, and to 2.1 +/- 0.5 s by flumazenil recovered to 0.6 +/- 0.1 s by naloxone. Expiratory time did not change during each drug administration in the two groups. The decrease of respiratory rate from 44 to 23 +/- 4 breaths.min-1 by morphine recovered to 37 +/- 5 breaths.min-1 by bicuculline and to 42 +/- 2 breaths.min-1 by naloxone. The decrease of respiratory rate from 45 +/- 3 to 22 +/- 6 breaths.min-1 by morphine, and to 18 +/- 4 breaths.min-1 by flumazenil recovered to 46 +/- 3 breaths.min-1 by naloxone. Amplitude of integrated phrenic nerve discharge increased to 125 +/- 42% by bicuculline and to 175 +/- 93% by naloxone compared to the baseline values. The decrease of amplitude to 54 +/- 18% by flumazenil recovered to 125 +/- 42% by naloxone. These results suggest that bicuculline not flumazenil antagonizes the respiratory depression of morphine by increasing the respiratory rate and respiratory movement.

Bupivacaine-induced convulsion is suppressed by MK-801.

BACKGROUND AND OBJECTIVES: Not only the facilitation of inhibitory synapses but also the suppression of excitatory synapses may be effective in treating convulsion induced by local anesthetics. The effects of MK-801, a N-methyl-D-aspartate (NMDA) receptor antagonist, on bupivacaine-induced convulsion and hemodynamic changes were studied. METHODS: Cortex and hippocampal (A4; L5.5; H8) electroencephalogram (EEG), heart rate, and mean arterial pressure were measured in 21 cats anesthetized with urethane. Blood samples were obtained when cats demonstrated arrhythmias, convulsed, and became hypotensive. In the control group (n = 7), bupivacaine was continuously infused until a hypotensive state of 40 mm/Hg was reached. In the MK-801 pretreated group (n = 7), MK-801 (0.5 mg/kg) was injected intravenously 15 minutes before the bupivacaine injection. In the MK-801 treatment group (n = 7), MK-801 (0.5 mg/kg) was injected intravenously at the appearance of convulsive EEG after the bupivacaine injection. RESULTS: Bupivacaine produced convulsion in the control group (17.1 +/- 2.4 microg/mL), but not in the MK-801 pretreated group. In the treatment group, convulsive EEG was suppressed gradually after injection of MK-801. The mean plasma bupivacaine concentrations (microg/mL) reaching arrhythmia and hypotension were 9.5 +/- 2.9 and 23.0 +/- 3.0, respectively, in the control group; 10.9 +/- 3.5 and 22.5 +/- 4.9, respectively, in the MK-801 pretreated group; and 7.5 +/- 1.6 and 21.0 +/- 3.0, respectively, in the MK-801 treatment groups. The mean arterial pressure and heart rate did not differ among the three groups. CONCLUSIONS: These results demonstrated that one mechanism of bupivacaine-induced convulsion is the excitatory neurotransmitter system in central nervous system and that MK-801 is effective in suppressing the convulsion without any effects on hemodynamics.

Haemodynamic effects of induction of general anaesthesia with propofol during epidural anaesthesia.

PURPOSE: To clarify whether propofol administration during thoracic or lumbar epidural anaesthesia intensifies the haemodynamic depression associated with epidural anaesthesia. METHODS: Patients (n = 45) undergoing procedures of similar magnitude were randomly divided into three study groups: a control group (n = 15) receiving general anaesthesia alone and two study groups undergoing thoracic (n = 15) and lumbar epidural anaesthesia (n = 15) before induction of general anaesthesia. All patients received 2 mg.kg-1 propofol at a rate of 200 mg.min-1, followed by a continuous infusion of 4 mg.kg-1.hr-1. Mean arterial blood pressure (MAP) and heart rate (HR) were measured at baseline, three minutes after induction, and one minute after tracheal intubation in all three groups and at 20 min after epidural anaesthesia was established in the thoracic and lumbar groups. RESULTS: Following epidural anaesthesia, MAP decreased from 94 +/- 14 (SD) at baseline to 75 +/- 11 mmHg (P < 0.0001) in the thoracic group and from 92 +/- 12 to 83 +/- 15 mmHg in the lumbar group. After propofol administration, MAP decreased further in the thoracic group to 63 +/- 9 mmHg (P = 0.0077) and to 67 +/- 10 mmHg (P = 0.0076) in the lumbar group. The MAP following propofol induction in the thoracic group (P < 0.0001) and in the lumbar group (P = 0.0001) was lower than MAP in the control group (81 +/- 9 mmHg). HR decreased only in response to thoracic epidural anaesthesia (P = 0.0066). CONCLUSION: The hypotensive effects of propofol are additive to those of epidural anaesthesia, resulting in a profound decrease in mean arterial pressure.

[The effects of cervical epidural anesthesia on epidural somatosensory evoked potentials and phrenic nerve activities].

We have investigated the effects of cervical epidural anesthesia on-phrenic nerve activity (PNA), and epidural somatosensory evoked potential (SSEP) elicited by stimulation of the radial nerve in pentobarbital anesthetized cats. PNA was suppressed significantly to 72% of control value 10 min after injection of 1% lidocaine and recovered to control value within 30 min. Following 2% lidocaine injection, PNA tended to be more suppressed than with 1% lidocaine to 57% and recovered to control value within 30 min. Peak latencies of P1, N1, P2, N2, and P3 before injection of 1% lidocaine were 1.05 (0.24), 1.20 (0.11), 1.51 (0.20), 1.56 (0.34), 2.71 (0.33) (msec (SD)), respectively. Though these latencies did not increase after injection of 1% lidocaine, injection of 2% lidocaine increased them significantly and these elevations continued for 120 min. The amplitude of N2 increased significantly after injection of 1% lidocaine and the amplitude of N2 and N2-P3 increased after injection of 2% lidocaine. These results indicate that 2% lidocaine blocked the sensory nerve and the effects continued much longer than the depression of PNA by cervical epidural anesthesia.

Epidural anesthesia enhances sympathetic nerve activity in the unanesthetized segments in cats.

To evaluate compensatory sympathetic excitation during epidural anesthesia, we measured cardiac and renal sympathetic nerve activity during thoracic or lumbar epidural anesthesia in cats. Thirteen cats were divided into three groups: five cats received thoracic epidural anesthesia, five received lumbar epidural anesthesia, and three received lumbar epidural anesthesia after the carotid sinus and vagoaortic nerves were severed (denervated lumbar group). Heart rate (HR), mean arterial pressure (MAP), and cardiac and renal sympathetic nerve activity were measured repeatedly after administration of a single dose of 0.1 mL/kg of 1% lidocaine via the epidural catheter. Epidural solution spread from a median of C-8 to T-6 in the thoracic epidural group, T-8 to L-3 in the lumbar epidural group, and T-7 to L-3 in the denervated lumbar group. During thoracic epidural anesthesia, HR, MAP, and cardiac sympathetic nerve activity decreased, while renal nerve activity increased. Similarly, HR, MAP, and renal sympathetic nerve activity decreased during lumbar epidural anesthesia, and cardiac activity increased. In the denervated lumbar group, HR, MAP, and renal sympathetic nerve activity decreased but cardiac activity remained unchanged. Sympathetic nerve activity in corresponding unanesthetized segments increased during thoracic or lumbar epidural anesthesia in association with significant decreases in MAP and HR. After severance of the carotid sinus and vagoaortic nerves, the absence of sympathetic excitation in the unanesthetized segments during lumbar epidural anesthesia suggests that the compensatory response is produced by the baroreceptor reflex response to anesthesia-induced hypotension.

[The effects of caffeine on the respiratory depression by morphine].

The effects of intravenous administration of caffeine on the discharge of the phrenic nerve were studied following vagotomy in 7 pentobarbital anesthetized mechanically ventilated rats. Morphine (0.4 mg.kg-1.min-1) was administered until the respiratory rate decreased to about half of the baseline respiratory rate. In those state, we first administered caffeine (20 mg.kg-1), intravenously and then administered naloxone (0.02 mg) intravenously. The increase of inspiratory time from 0.49 +/- 0.16 to 2.01 +/- 0.47 s by morphine recovered to 0.86 +/- 0.38 s by caffeine and 0.50 +/- 0.22 s by naloxone. Expiratory time did not change during each drug administration. The decrease of respiratory rate from 46.6 +/- 5.9 to 20.6 +/- 4.1 breaths.min-1 by morphine recovered to 39.6 +/- 6.1 breaths.min-1 by caffeine and 47.6 +/- 4.6 breaths.min-1 by naloxone. Amplitude of integrated phrenic nerve discharge increased to 117 +/- 32% by caffeine and 156 +/- 39% by naloxone compared to the baseline. These results suggest that caffeine acts as a respiratory stimulant on the respiratory depression by morphine.

Epidural fentanyl improves the onset and spread of epidural mepivacaine analgesia.

PURPOSE: To determine the extent of enhanced blockade by the combined use of epidural fentanyl and mepivacaine. We compared the onset of hypoalgesia, analgesia and the threshold of pressure pain. METHODS: Thirty patients were randomly divided into three groups. The fentanyl group received 10 ml saline containing 0.1 mg fentanyl, mepivacaine group received 10 ml mepivacaine 1% and a mixed group received 10 ml mepivacaine 1% with 0.1 mg fentanyl. All solutions, without epinephrine, were injected through an epidural catheter at T5-6 to T6-7. The change in sensation, loss of pin-prick and pain threshold sensation, measured by pressure algometer, were assessed at 2.5-min intervals for 15 min at the T4 dermatome. Spread of analgesia was determined at 15 min. RESULTS: Loss of pinprick was more rapid in the mixed, 11.0 +/- 2.7 (SD) min, than in the mepivacaine group, 15.0 +/- 2.9 min, (P < 0.05), although there was no difference in change of sensation. Pressure pain threshold increased with time in the mepivacaine (P < 0.05) and mixed (P < 0.05) groups. It was higher in the mixed than in the fentanyl and mepivacaine groups at 5, 7.5 and 10 min (P < 0.05). The lower level of analgesia was lower in the mixed than in the mepivacaine groups (P < 0.05). Blood pressure was unchanged in the three groups, but heart rate decreased at 7.5, 10, 12.5, and 15 min in the mepivacaine and mixed groups (P < 0.05). CONCLUSIONS: The addition of fentanyl to mepivacaine accelerates the onset of analgesia and enhances the analgesic effect of epidural block.

[Epidural anesthesia for patients with bronchial asthma].

The choice of epidural anesthesia for patients with bronchial asthma is controversial. We used epidural anesthesia during surgery in 16 cases of asthma. Epidural anesthesia produced by 1% or 2% lidocaine or mepivacaine without epinephrine did not induce asthmatic attack in any patients. After epidural block, general anesthesia was induced with midazolam and vecuronium and endotracheal tube was inserted in 9 patients. Asthmatic attack occurred in two patients. In one patient it occurred by the endotracheal intubation and in another patient during thyroidectomy under nitrous oxide - oxygen - sevoflurane anesthesia, although no attack was observed in 7 patients. Two patients were considered to be in severe state of bronchial asthma and they had been on steroid drug and inhalation therapy before surgery. Both patients recovered soon with antiasthmatic therapy. These results suggest that epidural anesthesia has little or no relevance to asthmatic attack.

[The level of analgesia with epidural injection of 2% mepivacaine using combined spinal and epidural analgesia].

We studied the level of analgesia obtained with epidural injection of 2% mepivacaine using combined spinal and epidural analgesia (CSE) and compared with the level obtained by epidural analgesia (EA). We inserted a catheter into the epidural space through the L2/3 interspace, and hyperbaric tetracaine was injected through the L3/4 interspace with 26G spinal needle in thirty patients for CSE. We checked the the level of analgesia 90 min after spinal anesthesia. After this, 23 out of 30 patients showed the extension of analgesia 15 min after injection of mepivacaine into the epidural catheter. In these patients, the level of analgesia and the dose of mepivacaine showed the regression line Y = 10.2-0.4X (Y: the level of analgesia, X: the dose of 2% mepivacaine, P < 0.05). We also showed the regression line Y = 16.1-0.7X (P < 0.05) for EA 15 min after epidural injection of mepivacaine in other 23 patients. To achieve the same level of analgesia of Th8 or Th6 with CSE and EA, the doses for epidural injection were calculated as 5.5 ml, 10.5 ml with CSE and 11.5 ml, 14.4 ml with EA, respectively. These results show that the epidural dose of local anesthetic for CSE is 1/2 to 2/3 of that necessary for EA.

[The effects of small dose midazolam in patients to reduce the uncomfortable feeling during epidural block procedure].

The effects of small dose midazolam to reduce the uncomfortable feeling during epidural block procedure were studied. All 160 patients (ASA I approximately II) were premedicated with intramuscular (I.M.) atropine sulfate 0.5 mg and hydroxyzine 50 mg. To relieve pain and anxiety during epidural block procedure, small dose midazolam (1 mg; 80 patients) was given intravenously in the operating room before epidural procedure. After epidural block, patients were anesthetized with nitrous oxide-oxygen-isoflurane or nitrous oxide-oxygen-sevoflurane. The following day, patient's self-assessments of pain during epidural block procedure were categorized as good and fair. Midazolam 1 mg was effective in the males (from 45% to 10%) and tended to allay patients' pain feeling in the females (from 40% to 23%). To investigate the uncomfortable feeling 1 further asked the patients whether epidural block procedure was more noxious than I.M. premedication or not. Noxious feeling was expressed in more I.M. premedicated patients (78%) than in epidural block procedure patients (48%). These results suggest that small dose midazolam is effective to relieve patients' uncomfortable feeling due to its sedative and antianxiety effects.

[The effects of pentazocine, diazepam and midazolam in patients to reduce the uncomfortable feeling during epidural block procedure].

The effects of pentazocine, diazepam and midazolam in 100 patients to reduce the uncomfortable feeling during epidural block procedure were studied. All patients (ASA I-II) were premedicated with intramuscular atropine sulfate 0.5 mg and hydroxyzine 50 mg. To relieve pain and anxiety during epidural block procedure, pentazocine (15 mg; 20 Cases or 30 mg; 20 Cases), diazepam (5 mg; 20 Cases) or midazolam (2.5 mg; 20 Cases) was given intravenously in the operating room before epidural procedure. After the epidural block, patients were anesthetized with nitrous oxide-oxygen-isoflurane or nitrous oxide-oxygen-sevoflurane. The following day, patients' self-assessments of pain during epidural block procedure were categorized as good and fair. The effects of drugs were compared between patients with im premedication only with patients with further iv administration. Patients with pentazocine 15 mg were similar to the patients given only im premedication. Pentazocine 30 mg and diazepam 5 mg tended to allay the patients' pain feeling. Midazolam 2.5 mg was effective producing anterograde amnesia and antianxiety effects. Small doses of midazolam were effective to relief patients' uncomfortable feeling.

Effects of abdominal surgery on somatosensory evoked potentials during nitrous oxide-enflurane anesthesia.

The effect of abdominal surgery on median nerve somatosensory evoked potentials (SEPs) was studied in 8 enflurane and nitrous oxide anesthesia (GOE) patients. We further compared the effect of epidural anesthesia. The first recording was done immediately prior to induction. Anesthesia was then induced with 5 mg.kg(-1) i.v. of thiopental and maintained with 1.0% enflurane, 66% N(2)O and 33% O(2). Before skin incision for abdominal surgery, the second recording was performed under GOE anesthesia and the third recording during surgery. Then 2% lidocaine was injected into the epidural space through a preinserted catheter, and after 15 min the fourth recording was obtained. The latencies of peaks N1, P2 and N2 and the amplitudes of N1-P2 and P2-N2 were measured. The latencies of N1, P2 and N2 increased and the amplitudes of N1-P2 and P2-N2 deceased significantly after the induction of anesthesia compared with the control values. During abdominal surgery the latencies of N1 and P2 decreased and the amplitudes of N1-P2 and P2-N2 increased. After epidural anesthesia, however, the latencies of N1 and P2 increased and the amplitudes of N1-P2 and P2-N2 decreased significantly and returned almost to the values recorded under preoperative GOE anesthesia. These phenomena indicated that the excitations produced by surgical stimulation in nerve ending might have been transmitted to the central nervous system via spinal nerves and blocked by epidural anesthesia.

[Effects of intravenous lidocaine administration on auditory brainstem response].

The effect of lidocaine on the auditory brainstem response (ABR) was investigated in 14 neurologically normal patients. Lidocaine 1.5 mg.kg-1.min-1 was injected intravenously over a 5 min period immediately followed by a continuous infusion of lidocaine 60 micrograms.kg-1.min-1. The seven peak latencies (waves I-VII) and amplitudes (waves I-VII) of the ABR were recorded before and 7-8 min after lidocaine infusion. Peak latencies of waves IV, V, VI, VII increased after epidural anesthesia compared with control values. Amplitudes of all waves were unchanged following intravenous lidocaine injection compared with control values. Interpeak latencies (I-II, II-III, III-IV, IV-V, V-VI, VI-VII), of every second peak (I-III, II-IV, III-V, IV-VI, V-VII), of every third peak except (III-VI, IV-VII) were unchanged compared with control values. Interpeak latencies of every fourth peak, of fifth peak increased after lidocaine injection compared with control values. The data obtained in this study with lidocaine injection were similar to the data after epidural anesthesia with lidocaine. One of the reason of the latency changes of ABR after epidural anesthesia was the systemic effect of lidocaine absorbed intravenously from the epidural space.

[Effects of intravenous lidocaine administration on median nerve somatosensory evoked potentials].

The effect of lidocaine on the median nerve somatosensory evoked potential (SSEP) was investigated in 14 neurologically normal patients. Lidocaine 1.5 mg.kg-1.min-1 was injected intravenously over a 5 min period immediately followed by a continuous infusion of lidocaine 60 micrograms.kg-1.min-1. The peak latencies (N1, P2, N2) and amplitudes (N1-P2, P2-N2) of the SSEP response over the sensory cortex were recorded before and after lidocaine infusion. The peak latencies in the control group and in the experimental group after lidocaine infusion of N1, P1, N2 were 19.4 +/- 1.0 msec, 19.7 +/- 1.0 msec (N1), 24.6 +/- 1.4 msec, 25.0 +/- 1.5 msec (P2), 32.5 +/- 2.5 msec, and 33.3 +/- 2.8 msec (N2), respectively. The amplitudes in the control group and in the experimental group after lidocaine infusion of N1-P2, P2-N2 were 9.0 +/- 4.3 microV, 10.3 +/- 4.7 microV (N1-P2), 7.2 +/- 3.6 microV, 8.6 +/- 3.9 microV (P2-N2), respectively. Peak latencies of all components (N1, P2, N2) increased after lidocaine infusion compared with control values. Amplitude of N1-P2 and P2-N2 increased significantly following lidocaine infusion compared with control values. The data obtained in this study suggested that the changes in peak latencies and amplitude after epidural anesthesia with lidocaine were due to the systemic effect of lidocaine absorbed intravenously from the epidural space.