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

BACKGROUND: The purpose of this study was to investigate the functional effects of temporalis myofascial flap after condylectomy, with or without disc removal, in elderly patients with anterior disc displacement (ADD) without reduction and an erosive condylar surface of the temporomandibular joint (TMJ). METHODS: A total of 15 joints from 11 elderly patients (71-78 years old) were included. The patients had pain, mandibular dysfunction symptoms, and unilateral or bilateral ADD as well as an erosive condylar surface of the TMJ. All patients underwent temporalis myofascial flap reconstruction after condylectomy, with or without disc removal. If the maximal mouth opening (MMO) remained <35 mm after condylectomy, coronoidotomy was also performed. Self-assessed pain and mandibular function, including MMO and protrusive and lateral movements, were evaluated. RESULTS: No patient experienced serious complications. Most measurements improved significantly after surgery compared to preoperatively. Most patients achieved nearly-normal mouth opening at 4 weeks after surgery. Although most patients felt discomfort during active postoperative physiotherapy, no patient reported serious pain during the follow-up period. CONCLUSION: Although nonsurgical therapy is often the first treatment choice for ADD without reduction of the TMJ, surgical intervention involving condylectomy and temporalis myofascial flap reconstruction may be a reasonable first option for elderly patients with an erosive condylar surface of the TMJ.
Aged* ; Follow-Up Studies ; Humans ; Joints ; Mouth ; Temporomandibular Joint

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: Intravenous lipid emulsion has been used to treat systemic toxicity of local anesthetics. The goals of this in vitro study were to determine the ability of two lipid emulsions (Intralipid(R) and Lipofundin(R) MCT/LCT) to reverse toxic dose local anesthetic-induced vasodilation in isolated rat aortas. METHODS: Isolated endothelium-denuded aortas were suspended for isometric tension recording. Vasodilation was induced by bupivacaine (3 x 10(-4) M), ropivacaine (10(-3) M), lidocaine (3 x 10(-3) M), or mepivacaine (7 x 10(-3) M) after precontraction with 60 mM KCl. Intralipid(R) and Lipofundin(R) MCT/LCT were then added to generate concentration-response curves. We also assessed vasoconstriction induced by 60 mM KCl, 60 mM KCl with 3 x 10(-4) M bupivacaine, and 60 mM KCl with 3 x 10(-4) M bupivacaine plus 1.39% lipid emulsion (Intralipid(R) or Lipofundin(R) MCT/LCT). RESULTS: The two lipid emulsions reversed vasodilation induced by bupivacaine, ropivacaine, and lidocaine but had no effect on vasodilation induced by mepivacaine. Lipofundin(R) MCT/LCT was more effective than Intralipid(R) in reversing bupivacaine-induced vasodilation. The magnitude of lipid emulsion-mediated reversal of vasodilation induced by high-dose local anesthetics was as follows (from highest to lowest): 3 x 10(-4) M bupivacaine-induced vasodilation, 10(-3) M ropivacaine-induced vasodilation, and 3 x 10(-3) M lidocaine-induced vasodilation. CONCLUSIONS: Lipofundin(R) MCT/LCT-mediated reversal of bupivacaine-induced vasodilation was greater than that of Intralipid(R); however, the two lipid emulsions equally reversed vasodilation induced by ropivacaine and lidocaine. The magnitude of lipid emulsion-mediated reversal of vasodilation appears to be correlated with the lipid solubility of the local anesthetic.
Amides ; Anesthetics, Local ; Animals ; Aorta ; Bupivacaine ; Emulsions ; Lidocaine ; Mepivacaine ; Rats ; Solubility ; Vasoconstriction ; Vasodilation

Alkaline Phosphatase ; Ascorbic Acid ; Bone Matrix ; Dental Papilla ; Dental Sac ; Dentin ; Dexamethasone ; Enamel Organ ; Humans ; Mandible ; Molar, Third ; Osteoblasts ; Osteocalcin ; RNA, Messenger ; Stem Cells ; Tooth ; Tooth Germ ; Trypsin ; Young Adult

Follow-Up Studies ; Humans ; Jaw ; Orthognathic Surgery

INTRODUCTION: Skeletal homeostasis is normally maintained by the stability between bone formation by osteoblasts and bone resorption by osteoclasts. However, the correlation between the inflammatory reaction and osteoblastic differentiation of cultured osteoprogenitor cells has not been fully investigated. This study examined the effects of inflammatory cytokines on the osteoblastic differentiation of cultured human periosteal-derived cells. MATERIALS AND METHODS: Periosteal-derived cells were obtained from the mandibular periosteum and introduced into the cell culture. After passage 3, the periosteal-derived cells were further cultured in an osteogenic induction Dulbecco's modified Eagle's medium (DMEM) medium containing dexamethasone, ascorbic acid, and beta-glycerophosphate. In this culture medium, tumor necrosis factor (TNF)-alpha with different concentrations (0.1, 1, and 10 ng/mL) or interleukin (IL)-1beta with different concentrations (0.01, 0.1, and 1 ng/mL) were added. RESULTS: Both TNF-alpha and IL-1beta stimulated alkaline phosphatase (ALP) expression in the periosteal-derived cells. TNF-alpha and IL-1beta increased the level of ALP expression in a dose-dependent manner. Both TNF-alpha and IL-1beta also increased the level of alizarin red S staining in a dose-dependent manner during osteoblastic differentiation of cultured human periosteal-derived cells. CONCLUSION: These results suggest that inflammatory cytokines TNF-alpha and IL-1beta can stimulate the osteoblastic activity of cultured human periosteal-derived cells.
Alkaline Phosphatase ; Anthraquinones ; Ascorbic Acid ; Bone Resorption ; Cell Culture Techniques ; Cytokines ; Dexamethasone ; Durapatite ; Glycerophosphates ; Homeostasis ; Humans ; Interleukins ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Periosteum ; Tumor Necrosis Factor-alpha

BACKGROUND: A toxic dose of bupivacaine produces vasodilation in isolated aortas. The goal of this in vitro study was to investigate the cellular mechanism associated with bupivacaine-induced vasodilation in isolated endotheliumdenuded rat aortas precontracted with phenylephrine. METHODS: Isolated endothelium-denuded rat aortas were suspended for isometric tension recordings. The effects of nifedipine, verapamil, iberiotoxin, 4-aminopyridine, barium chloride, and glibenclamide on bupivacaine concentration-response curves were assessed in endothelium-denuded aortas precontracted with phenylephrine. The effect of phenylephrine and KCl used for precontraction on bupivacaine-induced concentration-response curves was assessed. The effects of verapamil on phenylephrine concentration-response curves were assessed. The effects of bupivacaine on the intracellular calcium concentration ([Ca2+]i) and tension in aortas precontracted with phenylephrine were measured simultaneously with the acetoxymethyl ester of a fura-2-loaded aortic strip. RESULTS: Pretreatment with potassium channel inhibitors had no effect on bupivacaine-induced relaxation in the endothelium-denuded aortas precontracted with phenylephrine, whereas verapamil or nifedipine attenuated bupivacaine-induced relaxation. The magnitude of the bupivacaine-induced relaxation was enhanced in the 100 mM KCl-induced precontracted aortas compared with the phenylephrine-induced precontracted aortas. Verapamil attenuated the phenylephrine-induced contraction. The magnitude of the bupivacaine-induced relaxation was higher than that of the bupivacaine-induced [Ca2+]i decrease in the aortas precontracted with phenylephrine. CONCLUSIONS: Taken together, these results suggest that toxic-dose bupivacaine-induced vasodilation appears to be mediated by decreased calcium sensitization in endothelium-denuded aortas precontracted with phenylephrine. In addition, potassium channel inhibitors had no effect on bupivacaine-induced relaxation. Toxic-dose bupivacaine- induced vasodilation may be partially associated with the inhibitory effect of voltage-operated calcium channels.
4-Aminopyridine ; Animals ; Aorta* ; Barium ; Bupivacaine ; Calcium Channels ; Calcium* ; Glyburide ; Nifedipine ; Phenylephrine* ; Potassium Channels ; Rats* ; Relaxation ; Vasodilation* ; Verapamil