• The Korean Journal of Pain
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• v.33 no.4
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• pp.378-385
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• 2020

Background: The thoracic paravertebral block is an effective analgesic technique for postoperative pain management after breast surgery. The ultrasound-guided retrolaminar block (RLB) is a safer alternative to conventional paravertebral block. Thus, we assessed the analgesic efficacy of ultrasound-guided RLB for postoperative pain management after breast surgery. Methods: Patients requiring breast surgery were randomly allocated to group C (retrolaminar injection with saline) and group R (RLB with local anesthetic mixture). The RLB was performed at the level of T3 with local anesthetic mixture (0.75% ropivacaine 20 mL + 2% lidocaine 10 mL) under general anesthesia before the skin incision. The primary outcome was cumulative morphine consumption using intravenous patient-controlled analgesia (IV-PCA) at 24 hour postoperatively. The secondary outcomes were the visual analogue scale (VAS) scores at 1, 6, 24, and 48 hour postoperatively and the occurrence of adverse events and patient satisfaction after the surgery. Results: Forty-six patients were included, 24 in group C and 22 in group R. The cumulative morphine consumption using IV-PCA did not differ between the two groups (P = 0.631). The intraoperative use of remifentanil was higher in group C than in group R (P = 0.025). The resting and coughing VAS scores at 1 hour postoperatively were higher in group R than in group C (P = 0.011, P = 0.004). The incidence of adverse events and patient satisfaction was not significantly different between the two groups. Conclusions: A single injection of ultrasound-guided RLB did not reduce postoperative analgesic requirements following breast surgery.

• Journal of Oral Medicine and Pain
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• v.30 no.1
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• pp.25-34
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• 2005

A trigger point injection (TPI) has been reported to have an immediate analgesic effect, and to be one of the most widely employed treatment methods of myofascial pain. There are normal saline, local anesthetics, and steroids as the solutions frequently used in TPI. They can be used separately or in combination. Local anaesthetics have myotoxicity in proportion to its concentration. The purpose of this study was to evaluate microstructural changes in point of the myotoxic effects of the combined solution of lidocaine and dexamethasone (a local anesthetic and a steroid) after being injected into the muscle of BALB/c mice. And this study tested solutions with various concentration separately and in combination, to find out proper concentration of solution without muscular tissue damage. This study shows that lidocaine and dexamethasone combination is not histologically myotoxic in case of the concentration of lidocaine less than 1.5%. Also it is suggested from this study that this combined solution will have an analgesic and anti-inflammatory effect. Hereafter continuous study should be performed to reveal that these results can be applied to human when lidocaine and dexamethasone combination is used as an injection modality of TrP treatment.

• The Korean Journal of Pain
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• v.12 no.1
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• pp.36-42
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• 1999

Background: The current maximal recommended doses of lidocaine are 7 mg/kg with $5\;{\mu}g/ml$ of epinephrine. But in clinical practice, sometimes more doses of lidocaine are required to produce adequate regional anesthesia. Method: Twenty-two healthy women patients were divided into two groups and pretreated with valium 5 mg p.o., morphine 5 mg i.m., and midazolam 2 mg i.v. before operation. Of these, 7 mg/kg of 2% lidocaine with $5\;{\mu}g/ml$ of epinephrine were given to 11 patients epidurally. Initial 3 ml of epinephrine mixed lidocaine was given as a test dose and remaining doses were given 5 ml/30 sec with 3 min intervals. Radial arterial blood were drawn at 5, 10, 15, 20, 30, 45, 60, 90, 120 min to measure plasma lidocaine concentrations. After confirming all of the peak plasma concentrations of 7 mg/kg lidocaine were absolutely under $5\;{\mu}g/ml$, the other 11 patients were given 10 mg/kg of 2% lidocaine with $5\;{\mu}g/ml$ of epinephrine epidurally and blood samplings were taken according to the same method of 7 mg/kg group. The peak plasma concentration ($C_{max}$), time to reach to $C_{max}$ ($T_{max}$), time to reach to $T_4$, maximal sensory block level, systemic toxicity, and vital sign changes were investigated. Result: $C_{max}$ was significantly higher in 10 mg/kg group ($5.1{\pm}1.3\;{\mu}g/ml$) than 7 mg/kg group($3.3{\pm}0.5\;{\mu}g/ml$), but $T_{max}$ ($10.5{\pm}2.7$ min vs $10.9{\pm}3.1$ min) was not different. Time to reach $T_4$ was significantly shorter in 10 mg/kg group ($9.5{\pm}2.7$ min) than 7 mg/kg group ($12.7{\pm}3.2$ min) but maximal sensory block level ($T_{3.7{\pm}0.7}$ vs $T_{2.7{\pm}1.0}$) was not different. In four patients of 10 mg/kg group, peak plasma concentrations exceeded $5\;{\mu}g/ml$, but no systemic toxicities appeared. No significant vital sign changes were observed. Conclusion: The current maximal recommended doses of lidocaine, merely based on body weight are not always appropriate. Further studies are needed to determine more precise guideline of maximal doses that include various pharmacokinetic components.

• The Korean Journal of Pain
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• v.18 no.2
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• pp.198-203
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• 2005

Background: This study was designed to demonstrate the peripheral effect of ketamine on the synovia of the knee joint and evaluate the analgesic effect of an intraarticular ketamine injection following knee arthroscopy. Methods: In a double blind randomized study, 80 ASA class 1 or 2 patients were selected for elective arthroscopic knee surgery. The patients received either 20 ml of normal saline (Group C, n = 19), 20 ml of 0.5% ropivacaine (Group R, n = 21), 1 mg/kg of ketamine mixed with 20 ml of normal saline (Group K, n = 20) or 1 mg/kg of ketamine mixed with 20 ml of 0.5% ropivacaine (Group RK, n = 20), intraarticularly, just prior to wound closure. Postoperative pain was evaluated using a visual analogue scale (VAS 0 to 100) score at 1, 2, 6, 12, 24 and 48 hours after the intraarticular injection, with the side effects found in the four groups also evaluated. The patients' requests for rescue analgesic were recorded, total doses of tarasyn calculated and the overall patient satisfaction also evaluated. Results: The difference in the VAS scores for all time periods was not significant. The number of patients receiving rescue analgesics and the total doses received in Group C were greater than those for the other groups, but this was not significant. No side effects were observed in any of the patients. Conclusions: Ketamine and local anesthetics have been reported to have peripheral analgesic effects, with variable duration in the measurements of pain and hyperalgesia. However, we failed to demonstrate a peripheral analgesic effect on postoperative arthroscopic pain.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.297-305
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• 1998

This study used in vivo intracellular recording in rat hippocampus to evaluate the effect of lidocaine and MK-801 on the membrane properties and the synaptic responses of individual neurons to electrical stimulation of the commissural pathway. Cells in control group typically fired in a tonic discharge mode with an average firing frequency of $2.4{\pm}0.9$ Hz. Neuron in MK-801 treated group (0.2 mg/kg, i.p.) had an average input resistance of $3.28{\pm}5.7\;M{\Omega}$ and a membrane time constant of $7.4{\pm}1.8$ ms. These neurons exhibited $2.4{\pm}0.2$ ms spike durations, which were similar to the average spike duration recorded in the neurons of the control group. Slightly less than half of these neurons were firing spontaneously with an average discharge rate of $2.4{\pm}1.1$ Hz. The average peak amplitude of the AHP following the spikes in these groups was $7.4{\pm}0.6$ mV with respect to the resting membrane potential. Cells in MK-801 and lidocaine treated group (5 mg/kg, i.c.v.) had an average input resistance of $3.45{\pm}6.0\;M{\Omega}$ and an average time constant of $8.0{\pm}1.4$ ms. The cells were firing spontaneously at an average discharge rate of $0.6{\pm}0.4$ Hz. Upon depolarization of the membrane by 0.8 nA for 400 ms, all of the tested cells exhibited accommodation of spike discharge. The most common synaptic response contained an EPSP followed by early-IPSP and late-IPSP. Analysis of the voltage dependence revealed that the early-IPSP and late-IPSP were putative $Cl^--and\;K^+-dependent$, respectively. Systemic injection of the NMDA receptor blocker, MK-801, did not block synaptic responses to the stimulation of the commissural pathway. No significant modifications of EPSP, early-IPSP, or late-IPSP components were detected in the MK-801 and/or lidocaine treated group. These results suggest that MK-801 and lidocaine manifest their CNS effects through firing pattern of hippocampal pyramidal cells and neural network pattern by changing the synaptic efficacy and cellular membrane properties.

• The Korean Journal of Pain
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• v.29 no.4
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• pp.229-238
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• 2016

Background: The goal of this in vitro study was to investigate the effect of lipid emulsion on vasodilation caused by toxic doses of bupivacaine and mepivacaine during contraction induced by a protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDBu), in an isolated endothelium-denuded rat aorta. Methods: The effects of lipid emulsion on the dose-response curves induced by bupivacaine or mepivacaine in an isolated aorta precontracted with PDBu were assessed. In addition, the effects of bupivacaine on the increased intracellular calcium concentration ($[Ca^{2+}]_i$) and contraction induced by PDBu were investigated using fura-2 loaded aortic strips. Further, the effects of bupivacaine, the PKC inhibitor GF109203X and lipid emulsion, alone or in combination, on PDBu-induced PKC and phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17) phosphorylation in rat aortic vascular smooth muscle cells (VSMCs) was examined by western blotting. Results: Lipid emulsion attenuated the vasodilation induced by bupivacaine, whereas it had no effect on that induced by mepivacaine. Lipid emulsion had no effect on PDBu-induced contraction. The magnitude of bupivacaine-induced vasodilation was higher than that of the bupivacaine-induced decrease in $[Ca^{2+}]_i$. PDBu promoted PKC and CPI-17 phosphorylation in aortic VSMCs. Bupivacaine and GF109203X attenuated PDBu-induced PKC and CPI-17 phosphorylation, whereas lipid emulsion attenuated bupivacaine-mediated inhibition of PDBu-induced PKC and CPI-17 phosphorylation. Conclusions: These results suggest that lipid emulsion attenuates the vasodilation induced by a toxic dose of bupivacaine via inhibition of bupivacaine-induced PKC and CPI-17 dephosphorylation. This lipid emulsion-mediated inhibition of vasodilation may be partly associated with the lipid solubility of local anesthetics.