Interaction of lidocaine with reactive oxygen and nitrogen species

Günaydın, Berrin; Demiryürek, Abdullah Tuncay

doi:10.1046/j.1365-2346.2001.00931.x

Cited by 6 publications

(3 citation statements)

References 29 publications

(53 reference statements)

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“…This observation agrees with another study showing that LID at comparable concentrations decreased ROS generated in neutrophils 64. LID has also been reported to have a direct scavenging effect on peroxynitrite63 and on singlet oxygen 62. Therefore, the protective mechanisms of LID on mitochondrial function could be attributed to either blocking electron flow to down stream complexes (complex III), where greater ROS generation occurs during oxidative stress,14 to scavenging of mitochondrial ROS, or to both mechanisms.…”

Section: Discussionsupporting

confidence: 90%

Modulation of Mitochondrial Bioenergetics in the Isolated Guinea Pig Beating Heart by Potassium and Lidocaine Cardioplegia: Implications for Cardioprotection

Aldakkak

Stowe²,

Lesnefsky³

et al. 2009

Journal of Cardiovascular Pharmacology

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Mitochondria are damaged by cardiac ischemia-reperfusion (I/R) injury but can contribute to cardioprotection. We tested if hyperkalemic cardioplegia (CP) and lidocaine (LID) differently modulate mitochondrial (m) bioenergetics and protect hearts against I/R injury. Guinea pig hearts (n=71) were perfused with Krebs Ringer's (KR) solution before perfusion for 1 min just before ischemia with either CP ( ] and superoxide (ROS) were assessed at baseline, during the 1 min perfusion, and continuously during I/R. During the brief perfusion before ischemia, CP and LID decreased ROS and increased NADH without changing m [Ca 2+ ]. Additionally, CP decreased FAD. During ischemia, NADH was higher and ROS was lower after CP and LID, whereas m [Ca 2+ ] was lower only after LID. On reperfusion, NADH and FAD were more normalized, and m [Ca 2+ ] and ROS remained lower after CP and LID. Better functional recovery and smaller infarct size after CP and LID were accompanied by better mitochondrial function. These results suggest that mitochondria may be implicated, directly or indirectly, in protection by CP and LID against I/R injury.

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Section: Discussionsupporting

confidence: 90%

Modulation of Mitochondrial Bioenergetics in the Isolated Guinea Pig Beating Heart by Potassium and Lidocaine Cardioplegia: Implications for Cardioprotection

Aldakkak

Stowe²,

Lesnefsky³

et al. 2009

Journal of Cardiovascular Pharmacology

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show abstract

“…Inflammatory cells produce peroxynitrite by the reaction between nitric oxide and superoxide anion, both of which are present in inflamed tissues. Peroxynitrite is also known to react with lidocaine and bupivacaine [43, 44]. Ueno et al [41] focused on inflammatory peroxynitrite responsible for the local anesthetic failure of inflamed tissues.…”

Section: Change Of Membrane Interactivitymentioning

confidence: 99%

Interaction of Local Anesthetics with Biomembranes Consisting of Phospholipids and Cholesterol: Mechanistic and Clinical Implications for Anesthetic and Cardiotoxic Effects

Tsuchiya

Mizogami

2013

Anesthesiology Research and Practice

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Despite a long history in medical and dental application, the molecular mechanism and precise site of action are still arguable for local anesthetics. Their effects are considered to be induced by acting on functional proteins, on membrane lipids, or on both. Local anesthetics primarily interact with sodium channels embedded in cell membranes to reduce the excitability of nerve cells and cardiomyocytes or produce a malfunction of the cardiovascular system. However, the membrane protein-interacting theory cannot explain all of the pharmacological and toxicological features of local anesthetics. The administered drug molecules must diffuse through the lipid barriers of nerve sheaths and penetrate into or across the lipid bilayers of cell membranes to reach the acting site on transmembrane proteins. Amphiphilic local anesthetics interact hydrophobically and electrostatically with lipid bilayers and modify their physicochemical property, with the direct inhibition of membrane functions, and with the resultant alteration of the membrane lipid environments surrounding transmembrane proteins and the subsequent protein conformational change, leading to the inhibition of channel functions. We review recent studies on the interaction of local anesthetics with biomembranes consisting of phospholipids and cholesterol. Understanding the membrane interactivity of local anesthetics would provide novel insights into their anesthetic and cardiotoxic effects.

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“…[ 49 ] Such a sodium channel blockade also helps preserve myocardial adenosine triphosphate during ischemia and reperfusion due to the suppression of Na + /K + -ATPase activity and mitochondrial calcium loading. [ 45 , 50 ] Furthermore, lidocaine has been reported to reduce myocardial free radical generation [ 51 ] and apoptosis. [ 46 ] Those mechanisms may partly explain the association between intravenous lidocaine and a reduction in the length of hospital and ICU stay in the current meta-analysis.…”

Section: Discussionmentioning

confidence: 99%

Prophylactic effect of intravenous lidocaine against cognitive deficit after cardiac surgery: A PRISMA-compliant meta-analysis and trial sequential analysis

Hung

Liu

et al. 2022

Medicine

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Background: This study aimed at providing an updated evidence of the association between intraoperative lidocaine and risk of postcardiac surgery cognitive deficit. Methods: Randomized clinical trials (RCTs) investigating effects of intravenous lidocaine against cognitive deficit in adults undergoing cardiac surgeries were retrieved from the EMBASE, MEDLINE, Google scholar, and Cochrane controlled trials register databases from inception till May 2021. Risk of cognitive deficit was the primary endpoint, while secondary endpoints were length of stay (LOS) in intensive care unit/hospital. Impact of individual studies and cumulative evidence reliability were evaluated with sensitivity analyses and trial sequential analysis, respectively. Results: Six RCTs involving 963 patients published from 1999 to 2019 were included. In early postoperative period (i.e., 2 weeks), the use of intravenous lidocaine (overall incidence = 14.8%) was associated with a lower risk of cognitive deficit compared to that with placebo (overall incidence = 33.1%) (relative risk = 0.49, 95% confidence interval: 0.32–0.75). However, sensitivity analysis and trial sequential analysis signified insufficient evidence to arrive at a firm conclusion. In the late postoperative period (i.e., 6–10 weeks), perioperative intravenous lidocaine (overall incidence = 37.9%) did not reduce the risk of cognitive deficit (relative risk = 0.99, 95% confidence interval: 0.84) compared to the placebo (overall incidence = 38.6%). Intravenous lidocaine was associated with a shortened LOS in intensive care unit/hospital with weak evidence. Conclusion: Our results indicated a prophylactic effect of intravenous lidocaine against cognitive deficit only at the early postoperative period despite insufficient evidence. Further large-scale studies are warranted to assess its use for the prevention of cognitive deficit and enhancement of recovery (e.g., LOS).

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Interaction of lidocaine with reactive oxygen and nitrogen species

Abstract: Lidocaine can elicit direct scavenging activity at high concentrations that might be important at or near the site of injection in local anaesthetic use.

Cited by 6 publications

References 29 publications

Modulation of Mitochondrial Bioenergetics in the Isolated Guinea Pig Beating Heart by Potassium and Lidocaine Cardioplegia: Implications for Cardioprotection

Modulation of Mitochondrial Bioenergetics in the Isolated Guinea Pig Beating Heart by Potassium and Lidocaine Cardioplegia: Implications for Cardioprotection

Interaction of Local Anesthetics with Biomembranes Consisting of Phospholipids and Cholesterol: Mechanistic and Clinical Implications for Anesthetic and Cardiotoxic Effects

Prophylactic effect of intravenous lidocaine against cognitive deficit after cardiac surgery: A PRISMA-compliant meta-analysis and trial sequential analysis

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