BackgroundIntra-articular lidocaine is commonly used.PurposeThis study was conducted to determine whether short-term exposures to 1% and 2% lidocaine are toxic to articular chondrocytes, whether this is due to pH, and whether an intact articular surface is protective.Study DesignControlled laboratory study.MethodsFresh bovine articular chondrocytes in alginate bead cultures were treated with 1% or 2% lidocaine or buffered saline (pH 7.4, 7.0, and 5.0) for 15, 30, or 60 minutes. Chondrocytes were then analyzed for viability by flow cytometry 1 hour, 1 day, and 1 week later. Bovine osteochondral cores with and without the superficial 1 mm of cartilage removed were submerged in either 0.9% saline (pH 7.4) or in 1% or 2% lidocaine for 30 minutes and assessed for viability using fluorescent microscopy.ResultsChondrocyte viability decreased after just 15-minute exposures to 1% lidocaine. Longer exposures to 1% and 2% lidocaine further reduced chondrocyte viability. Chondrotoxicity of 2% lidocaine was greater th...

http://journals.sagepub.com/doi/pdf/10.1177/0363546507304719

Lidocaine Exhibits Dose- and Time-Dependent Cytotoxic Effects on Bovine Articular Chondrocytes In Vitro

Targeting of enteropathogenic Escherichia coli EspF to host mitochondria is essential for bacterial pathogenesis: critical role of the 16th leucine residue in EspF.

Local anesthetics are frequently used in fine-needle aspiration of thyroid lesions and locoregional control of persistent or recurrent thyroid cancer. Recent evidence suggests that local anesthetics have a broad spectrum of effects including inhibition of cell proliferation and induction of apoptosis in neuronal and other types of cells. In this study, we demonstrated that treatment with lidocaine and bupivacaine resulted in decreased cell viability and colony formation of both 8505C and K1 cells in a dose-dependent manner. Lidocaine and bupivacaine induced apoptosis, and necrosis in high concentrations, as determined by flow cytometry. Lidocaine and bupivacaine caused disruption of mitochondrial membrane potential and release of cytochrome c, accompanied by activation of caspase 3 and 7, PARP cleavage, and induction of a higher ratio of Bax/Bcl-2. Based on microarray and pathway analysis, apoptosis is the prominent transcriptional change common to lidocaine and bupivacaine treatment. Furthermore, lidocaine and bupivacaine attenuated extracellular signal-regulated kinase 1/2 (ERK1/2) activity and induced activation of p38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinase. Pharmacological inhibitors of MAPK/ERK kinase and p38 MAPK suppressed caspase 3 activation and PARP cleavage. Taken together, our results for the first time demonstrate the cytotoxic effects of local anesthetics on thyroid cancer cells and implicate the MAPK pathways as an important mechanism. Our findings have potential clinical relevance in that the use of local anesthetics may confer previously unrecognized benefits in the management of patients with thyroid cancer.

/pdf/local-anesthetics-induce-apoptosis-in-human-thyroid-cancer-3x6e4hdvf5.pdf

Local Anesthetics Induce Apoptosis in Human Thyroid Cancer Cells through the Mitogen-Activated Protein Kinase Pathway

During hypoxia in the CA1 region of the rat hippocampus, spreading-depression-like depolarization (hypoxic spreading depression or HSD) is accompanied by both a negative shift of the extracellular ...

/pdf/mitochondrial-and-intrinsic-optical-signals-imaged-during-44d22fwe3a.pdf

Mitochondrial and intrinsic optical signals imaged during hypoxia and spreading depression in rat hippocampal slices.

Background: Glenohumeral chondrolysis is the irreversible destruction of previously normal articular cartilage, occurring most commonly after shoulder surgery in young individuals The reported incidence of this complication has risen rapidly since the early 2000s As chondrolysis cannot be reversed, its occurrence can only be prevented by establishing and avoiding its causes

Methods: We analyzed all published cases of glenohumeral chondrolysis, including the relevant published laboratory data, to consolidate the available evidence on the causation of this complication by the postoperative intra-articular infusion of local anesthetic via a pain pump

Results: Analysis of the published evidence demonstrated a causal relationship between the infusion of local anesthetic and the development of glenohumeral chondrolysis The risk of this complication in shoulders receiving intra-articular infusions via a pain pump was significantly greater with higher doses of local anesthetic: twenty of forty-eight shoulders receiving high-flow infusions developed chondrolysis, whereas only two of twenty-five shoulders receiving low-flow infusions developed this complication (p = 00029) Eleven of twenty-two shoulders receiving 05% bupivacaine developed chondrolysis, whereas none of six shoulders receiving 025% bupivacaine developed this complication (p = 005) Of twenty-two shoulders infused with 05% bupivacaine, the eleven that developed chondrolysis had a mean pain pump delivery volume of 377 mL, whereas the eleven that did not develop chondrolysis had a mean volume of 187 mL (p = 0003) Among shoulders in which an intra-articular pain pump was used, the risk of chondrolysis was significantly greater when suture anchors were placed in the glenoid for labral repair (p < 0001)

Conclusions: The published evidence indicates that the preponderance of cases of glenohumeral chondrolysis can be prevented by the avoidance of the intra-articular infusion of local anesthetic via a pain pump

Level of Evidence: Therapeutic Level IV See Instructions for Authors for a complete description of levels of evidence

https://www.orthop.washington.edu/orthodev/drupal/sites/default/files/Published_evidence_demonstrating_the_causation_of_glenohumeral_chondrolysis_by_postoperative_infusion_of_local_anesthetic_via_a_pain_pump.pdf

Published Evidence Demonstrating the Causation of Glenohumeral Chondrolysis by Postoperative Infusion of Local Anesthetic Via a Pain Pump

Using the laser dye rhodamine 123, we demonstrated that local anaesthetics can reach mitochondria in cell culture and reversibly decrease, or even collapse, their transmembrane potential. This effect is highly dependent on the lipid-solubility of the local anaesthetic and can be facilitated by the presence of a lipophilic anion.

/pdf/effect-of-local-anaesthetics-on-mitochondrial-membrane-43kqgrdna5.pdf

Effect of local anaesthetics on mitochondrial membrane potential in living cells.

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Effect of local anaesthetics on mitochondrial membrane potential in living cells.