BACKGROUND: People with the Ehlers-Danlos Syndromes (EDS), a group of heritable disorders of connective tissue, often report experiencing dental procedure pain despite local anesthetic (LA) use. Clinicians have been uncertain how to interpret this apparent LA resistance, as comparison of EDS and non-EDS patient experience is limited to anecdotal evidence and small case series. The primary goal of this hypothesis-generating study was to investigate the recalled adequacy of pain prevention with LA administered during dental procedures in a large cohort of people with and without EDS. A secondary exploratory aim asked people with EDS to recall comparative LA experiences. METHODS: We administered an online survey through various social media platforms to people with EDS and their friends without EDS, asking about past dental procedures, LA exposures, and the adequacy of procedure pain prevention. Among EDS respondents who both received LA and recalled the specific LA used, we compared agent-specific pain prevention for lidocaine, procaine, bupivacaine, mepivacaine, and articaine. RESULTS: Among the 980 EDS respondents who had undergone a dental procedure LA, 88% (n = 860) recalled inadequate pain prevention. Among 249 non EDS respondents only 33% (n = 83) recalled inadequate pain prevention (P < 0.001 compared to EDS respondents). The agent with the highest EDS-respondent reported success rate was articaine (30%), followed by bupivacaine (25%), and mepivacaine (22%). CONCLUSIONS: EDS survey respondents reported nearly three times the rate of LA non-response compared to non-EDS respondents, suggesting that LAs were less effective in preventing their pain associated with routine office dental procedures.
Anesthesia, Local ; Anesthetics, Local ; Bupivacaine ; Carticaine ; Cohort Studies ; Connective Tissue ; Dental Care ; Ehlers-Danlos Syndrome ; Friends ; Humans ; Lidocaine ; Mepivacaine ; Procaine ; Social Media ; Surveys and Questionnaires

No abstract available.
Brachial Plexus Block* ; Brachial Plexus* ; Mepivacaine* ; Myoclonus* ; Upper Extremity*

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 ([Ca²⁺]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 [Ca²⁺]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.
Anesthetics, Local ; Animals ; Aorta ; Blotting, Western ; Bupivacaine* ; Calcium ; Fura-2 ; In Vitro Techniques ; Mepivacaine* ; Muscle, Smooth, Vascular ; Myosin-Light-Chain Phosphatase ; Phorbol 12,13-Dibutyrate ; Phosphorylation ; Protein Kinase C ; Rats ; Solubility ; Vasodilation*

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 ([Ca²⁺]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 [Ca²⁺]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.
Anesthetics, Local ; Animals ; Aorta ; Blotting, Western ; Bupivacaine* ; Calcium ; Fura-2 ; In Vitro Techniques ; Mepivacaine* ; Muscle, Smooth, Vascular ; Myosin-Light-Chain Phosphatase ; Phorbol 12,13-Dibutyrate ; Phosphorylation ; Protein Kinase C ; Rats ; Solubility ; Vasodilation*

BACKGROUND: Dexmedetomidine extends the duration of nerve block when administered perineurally together with local anesthetics by central and/or peripheral action. In this study, we compared the duration of nerve block between dexmedetomidine and epinephrine as an adjuvant to 1% mepivacaine in infraclavicular brachial plexus block. METHODS: Thirty patients, scheduled for upper limb surgery were assigned randomly to 3 groups of 10 patients each. We performed brachial plexus block using a nerve stimulator. In the control group (group C), patients received 40 ml of 1% mepivacaine. In group E, patients received 40 ml of 1% mepivacaine containing 200 microg of epinephrine as an adjuvant. In group D, patients received 40 ml of 1% mepivacaine containing 1 microg/kg of dexmedetomidine as an adjuvant. Sensory block duration, motor block duration, time to sense pain, and onset time were assessed. We also monitored blood pressure, heart rate, oxygen saturation and bispectral index. RESULTS: In group D and group E, sensory block duration, motor block duration and time to sense first pain were prolonged significantly compared to group C. However, there was no significant difference between group D and group E. CONCLUSIONS: Perineural 1 microg/kg of dexmedetomidine similarly prolonged nerve block duration compared to 200 microg of epinephrine, but slowed heart rate. Thus, dexmedetomidine is expected to be a good alternative as an adjuvant to local anesthesia in patients who are cautioned against epinephrine.
Anesthesia, Local ; Anesthetics, Local ; Blood Pressure ; Brachial Plexus* ; Dexmedetomidine* ; Epinephrine* ; Heart Rate ; Humans ; Mepivacaine* ; Nerve Block ; Oxygen ; Upper Extremity

BACKGROUND: To improve residual pain management in acute cervical radiculopathy treated with NSAIDs, the feasibility of early and repeated low-dose interscalene brachial plexus block (IS-BPB) needs to be assessed. METHODS: This was a prospective study on patients receiving NSAIDs (loxoprofen) for cervical radiculopathy of < or = 2-week onset. Pain was assessed using the visual analogue scale (VAS). A low-dose ultrasonography (USG)-guided IS-BPB (dexamethasone [1.65 mg; 0.5 ml] and mepivacaine [1%; 3.0 ml]) was performed at baseline and weekly thereafter for 4 weeks in an outpatient setting for the intervention group. All patients were evaluated using a visual satisfaction score (VSS) at week 4. Patients with baseline VAS scores < 70 (mild to moderate pain; MM group) and > or = 70 (severe pain; SE group) were compared to the controls receiving NSAIDs. RESULTS: A total of 316 IS-BPBs were performed in the intervention group. There was a significant difference in the decline in the VAS from week 0 to week 3 in the MM and SE groups (P < 0.05); however, from week 3 to week 4, the therapeutic effect exhibited no significant difference. Thirteen patients at week 2 (15.5%; MM: 27.7%; SE: 0%), 43 at week 3 (51.2%; MM: 83.0%; SE: 10.8%), and 47 at week 4 (56.0%; MM: 85.1%; SE: 18.9%) achieved a VAS score of < or = 20. Patient satisfaction was high, and the decrease in VAS scores in both groups was significant (P < 0.05) compared to the controls. CONCLUSIONS: Weekly, low-dose, USG-guided IS-BPB can be implemented for early pain relief in acute cervical radiculopathy, with high patient satisfaction.
Anti-Inflammatory Agents, Non-Steroidal* ; Brachial Plexus* ; Humans ; Mepivacaine ; Nerve Block ; Outpatients ; Pain Management ; Patient Satisfaction ; Prospective Studies ; Radiculopathy* ; Ultrasonography

BACKGROUND: Mepivacaine induces contraction or decreased blood flow both in vivo and in vitro. Vasoconstriction is associated with an increase in the intracellular calcium concentration ([Ca2+]i). However, the mechanism responsible for the mepivacaine-evoked [Ca2+]i increase remains to be determined. Therefore, the objective of this in vitro study was to examine the mechanism responsible for the mepivacaine-evoked [Ca2+]i increment in isolated rat aorta. METHODS: Isometric tension was measured in isolated rat aorta without endothelium. In addition, fura-2 loaded aortic muscle strips were illuminated alternately (48 Hz) at two excitation wavelengths (340 and 380 nm). The ratio of F340 to F380 (F340/F380) was regarded as an amount of [Ca2+]i. We investigated the effects of nifedipine, 2-aminoethoxydiphenylborate (2-APB), gadolinium chloride hexahydrate (Gd3+), low calcium level and Krebs solution without calcium on the mepivacaine-evoked contraction in isolated rat aorta and on the mepivacaine-evoked [Ca2+]i increment in fura-2 loaded aortic strips. We assessed the effect of verapamil on the mepivacaine-evoked [Ca2+]i increment. RESULTS: Mepivacaine produced vasoconstriction and increased [Ca2+]i. Nifedipine, 2-APB and low calcium attenuated vasoconstriction and the [Ca2+]i increase evoked by mepivacaine. Verapamil attenuated the mepivacaine-induced [Ca2+]i increment. Calcium-free solution almost abolished mepivacaine-induced contraction and strongly attenuated the mepivacaineinduced [Ca2+]i increase. Gd3+ had no effect on either vasoconstriction or the [Ca2+]i increment evoked by mepivacaine. CONCLUSIONS: The mepivacaine-evoked [Ca2+]i increment, which contributes to mepivacaine-evoked contraction, appears to be mediated mainly by calcium influx and partially by calcium released from the sarcoplasmic reticulum.
Animals ; Aorta* ; Calcium* ; Endothelium* ; Fura-2 ; Gadolinium ; Mepivacaine ; Nifedipine ; Rats* ; Sarcoplasmic Reticulum ; Vasoconstriction ; Verapamil

PURPOSE: Intravenous lipid emulsions have been used to treat the systemic toxicity of local anesthetics. The goal of this in vitro study was to examine the effects of lipid emulsions on the norepinephrine-mediated reversal of vasodilation induced by high doses of levobupivacaine, ropivacaine, and mepivacaine in isolated endothelium-denuded rat aorta, and to determine whether such effects are associated with the lipid solubility of local anesthetics. MATERIALS AND METHODS: The effects of lipid emulsions (0.30, 0.49, 1.40, and 2.61%) on norepinephrine concentration-responses in high-dose local anesthetic (6x10-4 M levobupivacaine, 2x10-3 M ropivacaine, and 7x10-3 M mepivacaine)-induced vasodilation of isolated aorta precontracted with 60 mM KCl were assessed. The effects of lipid emulsions on local anesthetic- and diltiazem-induced vasodilation in isolated aorta precontracted with phenylephrine were also assessed. RESULTS: Lipid emulsions (0.30%) enhanced norepinephrine-induced contraction in levobupivacaine-induced vasodilation, whereas 1.40 and 2.61% lipid emulsions enhanced norepinephrine-induced contraction in both ropivacaine- and mepivacaine-induced vasodilation, respectively. Lipid emulsions (0.20, 0.49 and 1.40%) inhibited vasodilation induced by levobupivacaine and ropivacaine, whereas 1.40 and 2.61% lipid emulsions slightly attenuated mepivacaine (3x10-3 M)-induced vasodilation. In addition, lipid emulsions attenuated diltiazem-induced vasodilation. Lipid emulsions enhanced norepinephrine-induced contraction in endothelium-denuded aorta without pretreatment with local anesthetics. CONCLUSION: Taken together, these results suggest that lipid emulsions enhance the norepinephrine-mediated reversal of local anesthetic-induced vasodilation at toxic anesthetic doses and inhibit local anesthetic-induced vasodilation in a manner correlated with the lipid solubility of a particular local anesthetic.
Amides/adverse effects ; Anesthetics, Local/*adverse effects ; Animals ; Bupivacaine/adverse effects/analogs & derivatives ; Emulsions/*chemistry/*therapeutic use ; Lipids/*chemistry ; Male ; Mepivacaine/adverse effects ; Norepinephrine/*therapeutic use ; Rats ; Rats, Sprague-Dawley ; Vasodilation/*drug effects

BACKGROUND: The aim of this study was to estimate the minimum effective volume (MEV) of 1.5% mepivacaine for ultrasound-guided supraclavicular block by placing the needle near the lower trunk of brachial plexus and multiple injections. METHODS: Thirty patients undergoing forearm and hand surgery received ultrasound-guided supraclavicular block with 1.5% mepivacaine. The initial volume of local anesthetic injected was 24 ml, and local anesthetic volume for the next patient was determined by the response of the previous patient. The next patient received a 3 ml higher volume in the case of the failure of the previous case. If the previous block was successful, the next volume was 3 ml lower. MEV was estimated by the Dixon and Massey up and down method. MEV in 95, 90, and 50% of patients (MEV95, MEV90, and MEV50) were calculated using probit transformation and logistic regression. RESULTS: MEV95 of 1.5% mepivacaine was 17 ml (95% confidence interval [CI], 13-42 ml), MEV90 was 15 ml (95% CI, 12-34 ml), and MEV50 was 9 ml (95% CI, 4-12 ml). Twelve patients had a failed block. Three patients received general anesthesia. Nine patients could undergo surgery with sedation only. Only one patient showed hemi-diaphragmatic paresis. CONCLUSIONS: MEV95 was 17 ml, MEV90 was 15 ml, and MEV50 was 9 ml. However, needle location near the lower trunk of brachial plexus and multiple injections should be performed.
Anesthesia, General ; Brachial Plexus ; Forearm ; Hand ; Humans ; Mepivacaine ; Needles

BACKGROUND: The ultrasound guidance in regional nerve blocks has recently been introduced and gaining popularity. Ultrasound-guided supraclavicular block has many advantages including the higher success rate, faster onset time, and fewer complications. The aim of this study was to examine the clinical data according to the varied volume of local anesthetics in the ultrasound-guided supraclavicular block. METHODS: One hundred twenty patients were randomized into four groups, according to the local anesthetic volume used: Group 35 (n = 30), Group 30 (n = 30), Group 25 (n = 30), and Group 20 (n = 30). Supraclavicular blocks were performed with 1% mepivacaine 35 ml, 30 ml, 25 ml, and 20 ml, respectively. The success rate, onset time, and complications were checked and evaluated. RESULTS: The success rate (66.7%) was lower in Group 20 than that of Group 35 (96.7%) (P < 0.05). The average onset times of Group 35, Group 30, Group 25, and Group 20 were 14.3 +/- 6.9 min, 13.6 +/- 4.5 min, 16.7 +/- 4.6 min, and 16.5 +/- 3.7 min, respectively. There were no significant differences. Horner's syndrome was higher in Group 35 (P < 0.05). CONCLUSIONS: In conclusion, we achieved 90% success rate with 30 ml of 1% mepivacaine. Therefore, we suggest 30 ml of local anesthetic volume for ultrasound-guided supraclavicular block.
Anesthetics, Local ; Horner Syndrome ; Humans ; Mepivacaine ; Nerve Block