Literature DB >> 26646023

Insulin Signaling in Bupivacaine-induced Cardiac Toxicity: Sensitization during Recovery and Potentiation by Lipid Emulsion.

Michael R Fettiplace1, Katarzyna Kowal, Richard Ripper, Alexandria Young, Kinga Lis, Israel Rubinstein, Marcelo Bonini, Richard Minshall, Guy Weinberg.   

Abstract

BACKGROUND: The impact of local anesthetics on the regulation of glucose homeostasis by protein kinase B (Akt) and 5'-adenosine monophosphate-activated protein kinase (AMPK) is unclear but important because of the implications for both local anesthetic toxicity and its reversal by IV lipid emulsion (ILE).
METHODS: Sprague-Dawley rats received 10 mg/kg bupivacaine over 20 s followed by nothing or 10 ml/kg ILE (or ILE without bupivacaine). At key time points, heart and kidney were excised. Glycogen content and phosphorylation levels of Akt, p70 s6 kinase, s6, insulin receptor substrate-1, glycogen synthase kinase-3β, AMPK, acetyl-CoA carboxylase, and tuberous sclerosis 2 were quantified. Three animals received Wortmannin to irreversibly inhibit phosphoinositide-3-kinase (Pi3k) signaling. Isolated heart studies were conducted with bupivacaine and LY294002-a reversible Pi3K inhibitor.
RESULTS: Bupivacaine cardiotoxicity rapidly dephosphorylated Akt at S473 to 63 ± 5% of baseline and phosphorylated AMPK to 151 ± 19%. AMPK activation inhibited targets downstream of mammalian target of rapamycin complex 1 via tuberous sclerosis 2. Feedback dephosphorylation of IRS1 to 31 ± 8% of baseline sensitized Akt signaling in hearts resulting in hyperphosphorylation of Akt at T308 and glycogen synthase kinase-3β to 390 ± 64% and 293 ± 50% of baseline, respectively. Glycogen accumulated to 142 ± 7% of baseline. Irreversible inhibition of Pi3k upstream of Akt exacerbated bupivacaine cardiotoxicity, whereas pretreating with a reversible inhibitor delayed the onset of toxicity. ILE rapidly phosphorylated Akt at S473 and T308 to 150 ± 23% and 167 ± 10% of baseline, respectively, but did not interfere with AMPK or targets of mammalian target of rapamycin complex 1.
CONCLUSION: Glucose handling by Akt and AMPK is integral to recovery from bupivacaine cardiotoxicity and modulation of these pathways by ILE contributes to lipid resuscitation.

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Year:  2016        PMID: 26646023      PMCID: PMC4718826          DOI: 10.1097/ALN.0000000000000974

Source DB:  PubMed          Journal:  Anesthesiology        ISSN: 0003-3022            Impact factor:   7.892


  75 in total

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4.  In vitro study on mechanisms of bupivacaine-induced depression of myocardial contractility.

Authors:  J J Eledjam; J E de La Coussaye; J Brugada; B Bassoul; J P Gagnol; J R Fabregat; C Massé; A Sassine
Journal:  Anesth Analg       Date:  1989-12       Impact factor: 5.108

5.  Mechanism for bupivacaine depression of cardiac conduction: fast block of sodium channels during the action potential with slow recovery from block during diastole.

Authors:  C W Clarkson; L M Hondeghem
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6.  Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage.

Authors:  James D Ross; Richard Ripper; William R Law; Malek Massad; Patricia Murphy; Lucas Edelman; Beth Conlon; Douglas L Feinstein; June W Palmer; Guido DiGregorio; Guy L Weinberg
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8.  Hypoglycemia enhances bupivacaine-induced cardiotoxicity in the rat.

Authors:  G P Lu; S S Schwalbe; G F Marx; G Batiller; R Limjoco
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9.  Epinephrine impairs lipid resuscitation from bupivacaine overdose: a threshold effect.

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Journal:  Local Reg Anesth       Date:  2018-08-08

Review 3.  Lipid Emulsion for Treating Local Anesthetic Systemic Toxicity.

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Journal:  Int J Med Sci       Date:  2018-05-14       Impact factor: 3.738

4.  Cardiac Arrest after Small Doses Ropivacaine: Local Anesthetic Systemic Toxicity in the Course of Continuous Femoral Nerve Blockade.

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5.  PRL/microRNA-183/IRS1 Pathway Regulates Milk Fat Metabolism in Cow Mammary Epithelial Cells.

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