Administration Of Bupivacaine Research Articles

Evaluation of chondrocyte death in canine osteochondral explants exposed to a 0.5% solution of bupivacaine

To evaluate chondrocyte death in canine articular cartilage exposed in vitro to bupivacaine with and without methylparaben and to compare viability for cartilage with intact or mechanically debrided surfaces. Both glenohumeral joints from 10 adult canine cadavers. 10 osteochondral cores were harvested from each of the 20 humeral heads; synovium and 1 core from each joint were examined to verify joint health, and the other 9 cores were exposed to canine chondrocyte culture medium (CCCM), a 0.5% solution of bupivacaine, or 0.5% solution of bupivacaine with methylparaben for 5, 15, or 30 minutes. For the superficial zone of surface-intact chondrocytes, bupivacaine with methylparaben caused a significantly higher percentage of chondrocyte death at 5 minutes (47.7%) than did bupivacaine (23.6%) or CCCM (25.4%). Bupivacaine (53.8%) and bupivacaine with methylparaben (62.5%) caused a significantly higher percentage of chondrocyte death at 30 minutes than did CCCM (20.0%). For the superficial zone of chondrocytes with debrided surfaces, bupivacaine with methylparaben caused a significantly higher percentage of chondrocyte death at 30 minutes (59%) than it did at 5 minutes (37.7%). Bupivacaine with methylparaben caused a significantly higher percentage of chondrocyte death at 30 minutes (59.0%) than did CCCM (28.9%). For middle and deep zones of chondrocytes, treatment solution and surface debridement had minimal effects on percentage of chondrocyte death. Bupivacaine and bupivacaine with methylparaben were cytotoxic to canine articular chondrocytes in vitro. Intra-articular administration of bupivacaine is not recommended for clinical use until additional studies are conducted.

Effectiveness of injection of local anesthetic into the retrobulbar space for postoperative analgesia following eye enucleation in dogs

To assess the efficacy of a retrobulbar bupivacaine nerve block for postoperative analgesia following eye enucleation in dogs. Randomized controlled trial. 22 dogs. Client-owned dogs admitted to the hospital for routine eye enucleation were enrolled with owner consent and randomly assigned to a treatment (bupivacaine hydrochloride) or control (saline [0.9% NaCl] solution) group. Baseline subjective pain scores were recorded. Anesthesia consisted of hydromorphone and midazolam preoperatively, thiopental or propofol for induction, and isoflurane in oxygen for maintenance. An inferior-temporal palpebral retrobulbar injection of either saline solution or bupivacaine was administered. Transpalpebral eye enucleation was performed. Pain scores were recorded at 0.25, 0.5, 1, 2, 4, 6, 8, and 24 hours after extubation (time 0) by observers masked to treatment groups. Dogs were given hydromorphone (0.2 mg/kg [0.09 mg/lb], IM or IV) as a rescue analgesic if the subjective pain score totaled >or= 9 (out of a maximum total score of 18) or >or= 3 in any 1 category. 9 of 11 control dogs required a rescue dose of hydromorphone, but only 2 of 11 dogs in the bupivacaine treatment group required rescue analgesia. Mean time to treatment failure (ie, administration of rescue analgesia following extubation) was 0.56 hours (95% confidence interval, 0.029 to 1.095 hours) for the 11 dogs that received hydromorphone. Retrobulbar administration of bupivacaine in dogs in conjunction with traditional premedication prior to eye enucleation was an effective form of adjunctive analgesia and reduced the need for additional postoperative analgesics.

Randomized controlled trial of bilateral superficial cervical plexus blockversusplacebo in thyroid surgery

Bilateral superficial cervical block during thyroid surgery can reduce postoperative pain but its value is unclear. This randomized clinical trial assessed the efficacy of such regional anaesthesia on postoperative pain after thyroid surgery performed under general anaesthesia. Patients undergoing thyroid surgery were randomized to one of four groups in a double-blind fashion. Patients received a cervical block with placebo or bupivacaine at the start or end of surgery. Postoperative pain, analgesic use and length of hospital stay were assessed. There were 159 patients eligible for analysis. The bupivacaine group had significantly less pain than the placebo group (P = 0.016). The timing of bupivacaine administration did not significantly influence pain (preoperative versus postoperative, P = 0.723). There was no difference between groups in the amount of analgesic used. Length of hospital stay was the same in the bupivacaine and placebo groups (P = 0.925) and when bupivacaine was administered at the beginning or end of surgery (P = 0.087). Bilateral superficial cervical block with bupivacaine combined with general anaesthesia significantly reduced postoperative pain after thyroid surgery. NCT00472446 (http://www.clinicaltrials.gov).

Pitfalls in Chronobiology

The duration of analgesia from epidural administration of local anesthetics to parturients has been shown to follow a rhythmic pattern according to the time of drug administration. We studied whether there was a similar pattern after intrathecal administration of bupivacaine in parturients. In the course of the analysis, we came to believe that some data points coincident with provider shift changes were influenced by nonbiological, health care system factors, thus incorrectly suggesting a periodic signal in duration of labor analgesia. We developed graphical and analytical tools to help assess the influence of individual points on the chronobiological analysis. Women with singleton term pregnancies in vertex presentation, cervical dilation 3 to 5 cm, pain score >50 mm (of 100 mm), and requesting labor analgesia were enrolled in this study. Patients received 2.5 mg of intrathecal bupivacaine in 2 mL using a combined spinal-epidural technique. Analgesia duration was the time from intrathecal injection until the first request for additional analgesia. The duration of analgesia was analyzed by visual inspection of the data, application of smoothing functions (Supersmoother; LOWESS and LOESS [locally weighted scatterplot smoothing functions]), analysis of variance, Cosinor (Chronos-Fit), Excel, and NONMEM (nonlinear mixed effect modeling). Confidence intervals (CIs) were determined by bootstrap analysis (1000 replications with replacement) using PLT Tools. Eighty-two women were included in the study. Examination of the raw data using 3 smoothing functions revealed a bimodal pattern, with a peak at approximately 0630 and a subsequent peak in the afternoon or evening, depending on the smoother. Analysis of variance did not identify any statistically significant difference between the duration of analgesia when intrathecal injection was given from midnight to 0600 compared with the duration of analgesia after intrathecal injection at other times. Chronos-Fit, Excel, and NONMEM produced identical results, with a mean duration of analgesia of 38.4 minutes (95% CI: 35.4-41.6 minutes), an 8-hour periodic waveform with an amplitude of 5.8 minutes (95% CI: 2.1-10.7 minutes), and a phase offset of 6.5 hours (95% CI: 5.4-8.0 hours) relative to midnight. The 8-hour periodic model did not reach statistical significance in 40% of bootstrap analyses, implying that statistical significance of the 8-hour periodic model was dependent on a subset of the data. Two data points before the change of shift at 0700 contributed most strongly to the statistical significance of the periodic waveform. Without these data points, there was no evidence of an 8-hour periodic waveform for intrathecal bupivacaine analgesia. Chronobiology includes the influence of external daily rhythms in the environment (e.g., nursing shifts) as well as human biological rhythms. We were able to distinguish the influence of an external rhythm by combining several novel analyses: (1) graphical presentation superimposing the raw data, external rhythms (e.g., nursing and anesthesia provider shifts), and smoothing functions; (2) graphical display of the contribution of each data point to the statistical significance; and (3) bootstrap analysis to identify whether the statistical significance was highly dependent on a data subset. These approaches suggested that 2 data points were likely artifacts of the change in nursing and anesthesia shifts. When these points were removed, there was no suggestion of biological rhythm in the duration of intrathecal bupivacaine analgesia.

Reversal of Bupivacaine-Induced Cardiac Electrophysiologic Changes by Two Lipid Emulsions in Anesthetized and Mechanically Ventilated Piglets

Accidental IV administration of bupivacaine can compromise cardiovascular function by inducing lethal arrhythmias whose hemodynamic consequences may be alleviated by lipid emulsions. However, little is known about the electrophysiologic effects of lipid emulsions. In this study, we assessed whether 2 different lipid emulsions can reverse cardiac electrophysiologic impairment induced by the IV administration of bupivacaine in anesthetized and mechanically ventilated piglets. Bupivacaine (4 mg . kg(-1)) was injected over a 30-second period in 26 piglets. Thirty seconds after the end of bupivacaine injection, 1.5 mL . kg(-1) saline solution for the control group, and long-chain triglyceride emulsion (LCT group) or a mixture of long-chain and medium-chain triglyceride emulsion (LCT/MCT group) were infused over 1 minute. Cardiac conduction variables and hemodynamic variables were monitored for 30 minutes after injection. Bupivacaine induced similar electrophysiologic and hemodynamic changes. After 3 minutes, His ventricle intervals (median and interquartiles) were 100 (85-105), 45 (35-55), and 53 (48-73) milliseconds in the control, LCT, and LCT/MCT groups, respectively (P < 0.001 between control and both lipid emulsion groups). Lipid emulsions also reversed the effects on QRS duration, atrial-His, and PQ (the onset of the P wave to the Q wave of the QRS complex) intervals. LCT/MCT emulsion restored the decrease in maximal first derivative of left ventricular pressure (P < 0.01 after 3 minutes versus control group). LCT and LCT/MCT emulsions reversed the lengthening of His ventricle, QRS, atrial-His, and PQ intervals induced by the IV injection of 4 mg . kg(-1) bupivacaine.

Is Chemical Incompatibility Responsible for Chondrocyte Death Induced by Local Anesthetics?

Background Chondrolysis associated with intra-articular administration of local anesthetics has been attributed to chondrocyte death induced by the local anesthetics. The mechanism of how the local anesthetics cause chondrocyte death is not clear. Purpose This study was conducted to determine whether and how the local anesthetics cause chondrocyte death. Study Design Controlled laboratory study. Methods Bovine articular chondrocytes in suspension culture were treated for 1 hour with phosphate-buffered saline or phosphate-buffered saline/medium mixture (as controls); 1% lidocaine alone; 0.25% to 0.5% bupivacaine alone; phosphate-buffered saline with pH values of 4.5, 3.8, 3.4, and 2.4; or mixtures of the local anesthetics and cell culture medium or human synovial fluid. Chondrocyte viability was analyzed by flow cytometry using the LIVE/DEAD Viability/Cytotoxicity Kit. Results In 1% lidocaine-alone or 0.25% to 0.5% bupivacaine-alone groups, the rate of cell death was 11.8% to 13.3% of bovine articular chondrocytes, whereas the phosphate-buffered saline control had 8.4% of cell death. Increased chondrocyte death was only found when the pH value of phosphate-buffered saline dropped to ≤3.4. In contrast, when bupivacaine was mixed with cell culture medium, needle-like crystals were formed, which was accompanied with 100% death of chondrocytes. Lidocaine did not form visible crystals when it was mixed with culture medium, but the mixtures caused death of over 96% of chondrocytes (P < .001). Conclusion Less than 5% of chondrocyte death was attributable to the anesthetics when applied to the cells alone or in phosphate-buffered saline—diluted solution. Acidity (as low as pH 3.8) or epinephrine in the anesthetic solutions could not account for chondrocyte death. However, chemical incompatibility between the local anesthetics and cell culture medium or human synovial fluid may be the cause of chondrocyte death. Clinical Relevance Intra-articular administration of lidocaine and bupivacaine is not an indicated usage of either anesthetic, although such a usage has become a common practice. Physicians should be aware of the potential incompatibility of the drug and synovial fluid.

Intramuscular Bupivacaine Injection Dose-dependently Increases Glutamate Release and Muscle Injury in Rats

Local anesthetics may cause reversible skeletal muscle injury, which is most common with bupivacaine. Glutamate is present in most skeletal muscles and may regulate muscular metabolic pathways. The aim of study was to examine the changes in intramuscular glutamate level and the severity of myopathy after intramuscular administration of bupivacaine. Twenty-four male Wistar rats were divided into four groups with six rats per group. A microdialysis probe was implanted in the right tibialis anterior (RTA) muscle in all rats. After equilibrating the microdialysis system for 2 hours, 0.2 mL of normal saline or 0.25%, 0.5% or 1% bupivacaine was injected into the RTA muscle and dialysate samples were collected every 30 minutes for 4 hours. Glutamate was measured by high-performance liquid chromatography. Three days later, the RTA muscle was dissected and the injection site was examined histologically to evaluate the severity of muscle damage on a four-point score, representing no damage to severe myonecrosis. Bupivacaine significantly increase the level of glutamate in a dose- dependent manner in the RTA muscle. Histological assessment of the RTA muscle after bupivacaine administration revealed dose-dependent damage (mean score: normal saline, 0; 0.25% bupivacaine, 1.2+/-0.6; 0.5% bupivacaine, 1.8+/-0.7; 1% bupivacaine, 2.4+/-0.8; p<0.05). A single intramuscular injection of bupivacaine induced dose-dependent increases in intramuscular glutamate levels and muscular damage.

A Randomised Controlled Trial of Hyperbaric Bupivacaine with Opioids, Injected as Either a Mixture or Sequentially, for Spinal Anaesthesia for Caesarean Section

It is common practice to mix opioids with hyperbaric bupivacaine in a single syringe before intrathecal injection of the mixture. Mixing these drugs may alter the density of the hyperbaric solution, affecting the spread of local anaesthetic and opioid. Forty-eight women having elective caesarean section under spinal anaesthesia were recruited to this double-blind, randomised trial. Group M (n=24) received 2 ml of 0.5% hyperbaric bupivacaine plus morphine 100 microg plus fentanyl 15 microg, mixed in a syringe prior to administration. Group S (n=24) received 2 ml of 0.5% bupivacaine through one syringe, followed by morphine 100 microg plus fentanyl 15 microg through a separate syringe. All patients received patient-controlled intravenous morphine for 24 hours postoperatively. Block characteristics, postoperative pain scores and morphine use were noted. The patients in Group M had higher levels of sensory block to cold than those in Group S (median T2 vs. T3) (P = 0.003). Five patients in Group M and none in Group S had a block to cold > or = T1 (P = 0.02). There was no difference between groups in the incidence of hypotension, need for vasopressor or side-effects. Morphine consumption was significantly higher in group M (13.3 +/- 11.2 vs. 6.2 +/- 7.2 mg, P = 0.015). Mixing of fentanyl and morphine with hyperbaric bupivacaine results in a higher level of sensory block than sequential administration of bupivacaine then opioid and may be associated with higher postoperative opioid requirement.

A Case of Cancer Pain Management by Long-Term Intrathecal PCA

Titration of oral or intravenous medication is the preferred method of pain management for most patients with cancer pain. However, some patients experience insufficient pain relief or considerable adverse effects from systemic opioids. For these reasons, the control of severe cancer pain continues to present a variety of challenges to clinicians. We report our experience of successfully managing cancer pain in a patient by means of long-term intrathecal administration of morphine, bupivacaine, and racemic ketamine via a patient-controlled delivery system. This therapy reduced the patient's nausea, vomiting, and somnolence, led to early hospital discharge, and increased her level of daily activity. There were no signs of motor paralysis, psychomimetic alteration, neurological dysfunction, or infection related to the intrathecal route during treatment. Intrathecal therapy is an effective treatment in terminally ill patients.

Recurrent spinal myoclonus after two episodes of spinal anesthesia at a 1-year interval -A case report-

Spinal myoclonus is an unusual, self-limiting, adverse event that may occur during spinal anesthesia. The exact cause and underlying biochemical mechanism of spinal myoclonus remain unclear. A few cases of spinal myoclonus have been reported after administration of intrathecal bupivacaine. We report a case in which spinal myoclonus recurred after two episodes of spinal anesthesia with bupivacaine at a 1-year interval in a 35-year-old woman. The myoclonus was acute and transient. The patient recovered completely, with no neurologic sequelae.

Dexamethasone attenuated bupivacaine-induced neuron injury in vitro through a threonine–serine protein kinase B-dependent mechanism

Bupivacaine is one of the amide type local anesthetics and is widely used for epidural anesthesia and blockade of nerves. Bupivacaine administration locally could result in neuron injury showing transient neurologic symptoms. Dexamethasone is a synthetic glucocorticoid and may exert cytoprotective properties against damage induced by some stimuli. In the present study, we evaluated the effects of dexamethasone on bupivacaine-induced toxicity in mouse neuroblastoma N2a cells. N2a cells were exposed to bupivacaine in the presence or absence of dexamethasone. After treatment, the cell viability, nuclear condensation, and lactate dehydrogenase levels were evaluated. Mitochondrial potential and Akt (threonine–serine protein kinase B) activation were also examined. In a separate experiment, we examined the effect of Akt inhibition by triciribine on cell viability following dexamethasone treatment. We also investigated whether dexamethasone could prevent lidocaine-induced neurotoxicity. Treatment of N2a cells with bupivacaine resulted in significant cell injury as evidenced by morphological changes, LDH leakage, and nuclear condensation. Pretreatment of the cells with dexamethasone significantly attenuated bupivacaine- and lidocaine-induced cell injury. Dexamethasone treatment prevented the decline of mitochondrial potential caused by bupivacaine and increased the levels of Akt phosphorylation. Importantly, pharmacological inhibition of Akt abolished the protective effect of dexamethasone against bupivacaine-induced cell injury. Our data suggest that pretreatment of neuroblastoma cells with dexamethasone exerts a protective effect on bupivacaine-induced neuronal cell injury. The mechanisms involve activating the Akt signaling pathway.

Discharge patterns of nociceptive primary afferent fibres in the rat coccygeal nerve after UV A-light exposure

We have shown that administration of the local anaesthetic bupivacaine into the base of rats’ tails prevents the development of hyperalgesia induced by UV A-light to a noxious thermal challenge, but not to noxious mechanical challenges. The aim of this study was to determine whether exposure of rats’ tails to UV A-light altered the responses of Aδ- and C-fibres innervating the tail to noxious mechanical and noxious thermal challenges. We dissected the right ventral coccygeal nerve in Sprague–Dawley rats that had their tails exposed to, or shielded from, UV A-light 24-h earlier. Single afferent Aδ- and C-fibres receptive fields were located and the response of a fibre to noxious blunt (3.9 N bar algometer) and punctate (rat toothed forceps) mechanical challenges, as well as a noxious thermal (49 °C) challenge was measured. In rats exposed to UV A-light, the peak firing rates and areas under the curve of post-challenge histograms of Aδ- and C-fibres evoked neural activity were increased when noxious blunt and punctate challenges were applied to the rats’ tails. However, the peak firing rate and areas under the curve of post-challenge histograms of C-fibre evoked neural activity, which were responsive to noxious thermal challenges, were not increased after UV A-light exposure. We have shown that the Aδ- and C-fibres that encode for noxious punctate and blunt challenges were sensitized after UV A-light exposure, but C-fibres responsible for encoding noxious thermal challenges were not sensitized by UV A-light exposure.

Effects of Dexmedetomidine Pretreatment on Bupivacaine Cardiotoxicity in Rats

We evaluated the effects of dexmedetomidine pretreatment on bupivacaine cardiotoxicity in anesthetized rats. Sixteen Wistar-Albino male rats (300-400 g) were anesthetized with ketamine. Electrocardiographic and invasive blood pressure monitoring were performed, and the results were continuously recorded. The rats were randomized into 2 groups. In group D, rats were pretreated with intravenous dexmedetomidine at a dose of 10 Kg/kg (n = 8), whereas in group S, rats were pretreated with intravenous saline (n = 8). Fifteen minutes later, bupivacaine was infused at a rate of 3 mg/kg per minute until cardiac asystole occurred. The timing of specific cardiotoxic events (a 25%, 50%, and 75% reductions of mean arterial pressure and heart rate as well as occurrence of the first arrhythmia and asystole) was recorded. Dexmedetomidine pretreatment reduced the heart rates and mean arterial pressures of the rats who received it (P G 0.05). Dexmedetomidine pretreatment before bupivacaine administration also significantly increased the time to the 25%, 50%, and 75% reductions in mean arterial pressure and the time to the 25% and 50% reductions in heart rate (P G 0.05). In addition, dexmedetomidine significantly increased the time to first arrhythmia and time to asystole (P G 0.05) in the rats who received it before receiving bupivacaine. Dexmedetomidine pretreatment delays the effects of bupivacaine cardiotoxicity.

Comparison of intrathecal fentanyl and sufentanil in low-dose dilute bupivacaine spinal anaesthesia for transurethral prostatectomy

The administration of low-dose bupivacaine can limit the distribution of spinal block to reduce adverse haemodynamic effects. Intrathecal opioids can enhance analgesia in combination with subtherapeutic doses of local anaesthetics. We aimed at comparing the efficacy of intrathecal fentanyl and sufentanil with low-dose diluted bupivacaine for transurethral prostatectomy (TURP) in elderly patients. Seventy patients undergoing TURP were randomly allocated into two groups. Group F (n=35) received fentanyl 25 microg+bupivacaine 0.5% (0.8 ml)+normal saline 0.3 ml and Group S (n=35) received sufentanil 5 microg+bupivacaine 0.5% (0.8 ml)+normal saline 0.7 ml--in total, bupivacaine 0.25% (1.6 ml) intrathecally. Onset and duration of the sensory block, the degree of the motor block, side-effects, and the perioperative analgesic requirements were assessed. The median peak level of the sensory block was significantly higher in Group S than in Group F (P=0.049). Group S required fewer perioperative analgesics than Group F (P=0.008). The time to the first analgesic request was longer in Group S (P=0.025). There were no differences between the groups for the onset and recovery time of the sensory block, degree of the motor block, quality of anaesthesia, or adverse effects. Low-dose diluted bupivacaine with fentanyl 25 microg or sufentanil 5 microg can provide adequate anaesthesia without haemodynamic instability for TURP in elderly patients. However, sufentanil was superior to fentanyl in the quality of the spinal block produced.

α-Lipoic acid prevents bupivacaine-induced neuron injury in vitro through a PI3K/Akt-dependent mechanism

Background Bupivacaine is an amide type local anesthetic which is widely used for epidural anesthesia and nerve blockade in patients. However, local administration of bupivacaine could cause neuron injury showing transient neurologic symptoms. α-Lipoic acid (LA) was shown to protect nerve cells from substance-induced injury. We hypothesized that LA administration could attenuate bupivacaine-induced neurotoxicity. Methods To evaluate our hypothesis, we treated mouse neuroblastoma N2a cells with LA 30 min before the cells were exposed to bupivacaine. We evaluated cellular injury by examination of cell viability, morphology changes, nuclear condensation, and Annexin V staining. We also examined the levels of intracellular reactive oxygen species (ROS) and activation of PI3K/Akt signaling pathway. In a separate experiment, we determined the effect of Akt inhibition on cell viability in the presence of LA and bupivacaine. Results Bupivacaine treatment significantly induced cell injury as evidenced by decreased cell viability, increased nuclear condensation and Annexin V staining. Administration of LA significantly attenuated bupivacaine-induced cell injury. In addition, LA treatment increased the levels of phospho-Akt and phospho-GSK3β and attenuated bupivacaine decreased the levels of ROS. More significantly, pharmacological inhibition of Akt abolished the LA-induced protection from bupivacaine-caused cell injury. Conclusions Our findings suggest that pretreatment of neuroblastoma cells with LA protected neural cells from bupivacaine-induced injury. The mechanisms involve activation of the PI3K/Akt signaling pathway.

High intrathecal bupivacaine for severe pain in the head and neck

Severe pain in the head and neck is associated with a lowered quality of life and conventional pain therapy often does not provide adequate relief. The aims of this study were to investigate the efficacy, pain relief, benefits and adverse effects of intracisternal or high cervical (IHC) administration of bupivacaine in patients with severe pain in the head, neck and face regions. Between 1990 and 2005, 40 patients (age 27-84 years) were treated with continuous IHC infusions of bupivacaine for various non-cancer (n=15) or cancer-related (n=25) refractory pain conditions (duration 1 month-18 years) in the head, neck, mouth and shoulder regions. Visual analogue scale scores and opioid requirements decreased markedly after the start of the treatment and remained lowered throughout the study. No tachyphylaxis for bupivacaine was observed. Major side effects were few and most often transient. Most patients showed unchanged or improved mobility. There was no mortality, neurological damage or other severe events attributable to procedures in the study protocol. For patients with severe and refractory pain in areas innervated by cranial and upper cervical nerves, cervical high spinal analgesia can provide safe and effective analgesia.

Bupivacaine concentrations in the lumbar cerebrospinal fluid of patients during spinal anaesthesia

Data on bupivacaine concentrations in the cerebral spinal fluid (CSF) during spinal anaesthesia are scarce. The purpose of this study was to determine the concentration of bupivacaine in the lumbar CSF of patients with an adequate level of spinal anaesthesia after injection of plain bupivacaine 0.5%. Sixty patients with an adequate level of spinal block after standardized administration of plain bupivacaine 20 mg in men and of 17.5 mg in women were studied. To measure the CSF bupivacaine concentration, we performed a second lumbar spinal puncture and obtained a CSF sample at a randomized time point 5-45 min after the bupivacaine injection. In addition, we calculated the half-life of bupivacaine in the CSF and tested the hypothesis that the level of spinal block is related to the lumbar CSF bupivacaine concentration. Men and women had CSF bupivacaine concentrations ranging from 95.4 to 773.0 microg ml(-1) (median 242.4 microg ml(-1)) and from 25.9 to 781.0 microg ml(-1) (median 187.6 microg ml(-1)), respectively. The large variability of bupivacaine concentrations obtained at similar times after subarachnoid administration made calculation of a meaningful half-life of bupivacaine in CSF impossible. There was no association between CSF bupivacaine concentration and spinal block level, and CSF bupivacaine concentrations for the same spinal block level differed between patients by six-fold. There is a large variability of CSF bupivacaine concentrations in patients with an adequate level of spinal anaesthesia.

Spinal Anesthesia With Sequential Administration of Plain and Hyperbaric Bupivacaine Provides Satisfactory Analgesia With Hemodynamic Stability in Cesarean Section

Spinal Anesthesia With Sequential Administration of Plain and Hyperbaric Bupivacaine Provides Satisfactory Analgesia With Hemodynamic Stability in Cesarean Section

Many Recipes for the Same Dish: Can Minor Modification Cause Major Improvement?

Department of Anaesthesia, Hull Royal Infirmary, Hull, UK Editors Note: The following is an abstract of an editorial comment on the paper abstracted above: (Cesur et al. Spinal Anesthesia with Sequential Administration of Plain and Hyperbaric Bupivacaine Provides Satisfactory Analgesia with Hemodynamic Stability in Cesarean Section).

A comparison of epidural anaesthesia with lignocaine, bupivacaine and a lignocaine-bupivacaine mixture in cats

A mixture of 2% lignocaine (LIG) and 0.5% bupivacaine (BUP), at respective dose rates of 2 mg/kg and 0.5 mg/kg (LIG-BUP), was compared to LIG (4 mg/kg) and BUP (1 mg/kg) for lumbosacral epidural anaesthesia in 5 sedated cats. Each cat received all 3 treatment regimens at 1-week intervals. The cats were premedicated with an intramuscular injection of atropine sulphate (0.04 mg/kg) and ketamine hydrochloride (10 mg/kg). Onset and duration of analgesia, and time to walking were determined. Associated changes in heart rate (HR), respiratory frequency (fR) and rectal temperature (RT) were recorded. Onset of analgesia with epidurally administered LIG-BUP (4.5 +/- 0.7 min), LIG (3.9 +/- 1.0 min) and BUP (5.0 +/- 1.0 min) was similar. Duration of analgesia with LIG-BUP (49.4 +/- 4.5 min) was significantly (P<0.05) longer than with LIG (40.2 +/- 1.0 min) but shorter than with BUP (79.4 +/- 6.3 min). There were no significant differences in times to standing with LIG-BUP (26.3 +/- 6.4 min), LIG (20.4 +/- 4.7 min) and BUP (22.6 +/- 10.3 min). Minimal changes were observed in HR, fR and RT. In conclusion, duration of analgesia produced by LIG-BUP was shorter compared with BUP but longer compared with LIG. Neither LIG nor LIG-BUP has any advantage over epidural BUP in terms of onset of analgesia, time to standing and physiological responses. Therefore, lumbosacral epidural administration of BUP appears to be the best choice for a long surgical procedure lasting more than 1 hour when compared with either LIG or LIG-BUP.