Total Local Anesthetic Administered Is Integral to the Syndrome of Local Anesthetic Systemic Toxicity

Petrar, Steven; Montemurro, Trina

doi:10.1097/aln.0000000000000425

Cited by 5 publications

(3 citation statements)

References 2 publications

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“…Despite the wide application and good efficacy of local anaesthetics, local anaesthesia‐induced neuron injury, and neurotoxicity remain a problem 1,2 . It has been reported that local anaesthetics can contribute to perioperative nerve damage 3,4 .…”

Section: Introductionmentioning

confidence: 99%

DJ‐1 plays a neuroprotective role in SH‐SY5Y cells by modulating Nrf2 signaling in response to lidocaine‐mediated oxidative stress and apoptosis

Xue

Wang

2020

The Kaohsiung J of Med Scie

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To investigate the effects of DJ‐1 on lidocaine‐induced cytotoxicity in neurons and the link with Nrf2 signaling, SH‐SY5Y cells were treated with 1, 4, 8, and 16 mM lidocaine. Cell viability was measured by MTT assay, and apoptosis was measured by flow cytometry analysis. The mitochondrial membrane potential, reactive oxygen species (ROS) levels, lipid peroxidation (MDA), and GSH/GSSG ratio were determined with specific kits. Expression of DJ‐1, Nrf2, and Nrf2 downstream signaling proteins (glutathione peroxidase [GPx], heme oxygenase‐1 [HO‐1], catalase [CAT], and glutathione reductase [GR]), was determined by western blot and qRT‐PCR. The cell viability was dramatically decreased, while levels of apoptosis, ROS and Cys106‐oxidized DJ‐1 were significantly enhanced following treatment with lidocaine (concentration 4‐16 mM), and increases were observed in a dose‐dependent manner. After treatment with 8 mM lidocaine, DJ‐1, and nuclear Nrf2, as well as antioxidative stress‐related proteins, GPx, GR, HO‐1, and CAT, were all significantly inhibited. Overexpression of DJ‐1 suppressed lidocaine‐induced apoptosis and oxidative stress in SH‐SY5Y cells and activated Nrf2 signalling at the same time, and these effects were reversed by the inhibition of Nrf2. DJ‐1 could protect SH‐SY5Y cells from lidocaine‐induced apoptosis through inhibition of oxidative stress via Nrf2 signaling.

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Section: Introductionmentioning

confidence: 99%

DJ‐1 plays a neuroprotective role in SH‐SY5Y cells by modulating Nrf2 signaling in response to lidocaine‐mediated oxidative stress and apoptosis

Xue

Wang

2020

The Kaohsiung J of Med Scie

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“…Performing a patient assessment allows the practitioner to identify allergies and comorbidities that might affect the absorption of the local anesthetic and to obtain baseline measures of the patient's vital signs, pain, anxiety, and level of consciousness (Ogg, 2021). Patient factors (eg, cardiac, renal, hepatic dysfunction) may alter the total local anesthetic dose calculations (Garcia-Rodriguez & Spiegel, 2018;Khatri et al, 2010;Petrar & Montemurro, 2014).…”

Section: Patient Assessmentmentioning

confidence: 99%

Safe and Effective Use of Local Anesthetics

Van Wicklin

2024

Plastic and Aesthetic Nursing

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“…However, the neuron damage and neurotoxicity they cause remain a problem. 1 Clinical studies have shown that prolonged or high-dose exposure to local anesthetics can cause spinal neurotoxicity or cause irreversible neurological dysfunctions. A growing body of evidence shows that bupivacaine, which is frequently preferred due to its effect of blocking the impulse transmission in the nerves by inhibiting the permeability of sodium ions, causes severe neurotoxicity in both animals and humans through various neuronal signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Kapsaisin apoptozu düzenleyerek SH-SY5Y hücrelerinde bupivakain anestezisinin neden olduğu nörotoksisiteyi hafifletmektedir

ALTUN

2022

Acta Med Nicomedia

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Objective: Bupivacaine administered for local anesthesia can cause critical neurotoxicity and neurological dysfunctions. Any substance that can reduce bupivacaine-mediated toxic effects will be of great interest during surgical procedures and in the pain management process. In this context, we evaluated capsaicin, an alkaloid of Capsicum annuum (cayenne pepper), which has been intensively researched for its neuroprotective effect due to its various biological effects such as cardioprotective, antiinflammatory, analgesic, thermogenic, and benefits on the gastrointestinal tract. Methods: In this study, we researched the in vitro effect of capsaicin in SH-SY5Y cells with a model of bupivacaine-mediated neurotoxicity. Cell proliferation assay was handled by XTT, and apoptosis was determined by flow cytometry analysis. Results: We observed a notable increase in apoptosis induction with a significant decrease in the viability of cells exposed to bupivacaine at 1 mM. We found that bupivacaine-mediated cytotoxicity was reduced when increasing concentrations of capsaicin were applied to bupivacaine-treated cells. At the same time, capsaicin also reduced apoptosis in SH-SY5Y cells exposed to bupivacaine. Conclusion: According to our results, it is thought that the administration of capsaicin against bupivacaine-mediated neurotoxicity may be an alternative neuroprotective agent by suppressing the apoptosis response in neurons.

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Total Local Anesthetic Administered Is Integral to the Syndrome of Local Anesthetic Systemic Toxicity

Cited by 5 publications

References 2 publications

DJ‐1 plays a neuroprotective role in SH‐SY5Y cells by modulating Nrf2 signaling in response to lidocaine‐mediated oxidative stress and apoptosis

DJ‐1 plays a neuroprotective role in SH‐SY5Y cells by modulating Nrf2 signaling in response to lidocaine‐mediated oxidative stress and apoptosis

Safe and Effective Use of Local Anesthetics

Kapsaisin apoptozu düzenleyerek SH-SY5Y hücrelerinde bupivakain anestezisinin neden olduğu nörotoksisiteyi hafifletmektedir

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