Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity

Hoegberg, Lotte Christine Groth; Bania, Theodore C.; Lavergne, Valéry; Bailey, Benoît; Turgeon, Alexis F.; Thomas, Simon; Morris, Martin; Miller-Nesbitt, Andrea; Mégarbane, Bruno; Magder, Sheldon; Gosselin, Sophie; Workgroup, Lipid Emulsion

doi:10.3109/15563650.2015.1121270

Cited by 83 publications

(58 citation statements)

References 108 publications

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“…Intralipid is mainly used to treat local anaesthetic systemic toxicity, and Lipofundin MCT/LCT is sometimes used to treat local anaesthetic systemic toxicity [19][20][21][22][23][24]. Although lipid emulsion alleviates the toxic dose of bupivacaine-mediated inhibition of vasodilation induced by the K ATP channel agonist levcromakalim primarily by scavenging effects regarded as indirect action, Intralipid may provide a more favourable effect than Lipofundin MCT/LCT on the maintenance of vasodilation induced by K ATP channel activation mediated through the pathophysiological state caused by local anaesthetic systemic toxicity [25].…”

Section: Discussionmentioning

confidence: 99%

Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release

Lee

Kang

et al. 2020

IJMS

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The goal of this study was to examine the effect of lipid emulsion on the vasodilation induced by ATP-sensitive potassium (KATP) channels in isolated rat aortae and the underlying mechanism. The effects of Intralipid, containing 100% long-chain fatty acids, and Lipofundin MCT/LCT, containing 50% long-chain fatty acids plus 50% medium-chain fatty acids, on the vasodilation induced by levcromakalim in endothelium-intact aorta with or without NW-nitro-L-arginine methyl ester (L-NAME) and in endothelium-denuded aorta were examined. The effects of L-arginine, L-NAME, glibenclamide, and Lipofundin MCT/LCT, alone or combined, on the levcromakalim-induced vasodilation were examined. Lipofundin MCT/LCT inhibited the levcromakalim-induced vasodilation of isolated endothelium-intact aortae, whereas Intralipid did not. In addition, Lipofundin MCT/LCT had no effect on the levcromakalim-induced vasodilation of endothelium-denuded rat aortae and endothelium-intact aortae with L-NAME. L-arginine and Lipofundin MCT/LCT produced more levcromakalim-induced vasodilation than Lipofundin MCT/LCT alone. Glibenclamide inhibited levcromakalim-induced vasodilation. Levcromakalim did not significantly alter endothelial nitric oxide synthase phosphorylation, whereas Lipofundin MCT/LCT decreased cyclic guanosine monophosphate. Lipofundin MCT/LCT did not significantly alter levcromakalim-induced membrane hyperpolarization. Taken together, these results suggest that Lipofundin MCT/LCT inhibits the vasodilation induced by levcromakalim by inhibiting basally released endothelial nitric oxide, which seems to occur through medium-chain fatty acids.

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Section: Discussionmentioning

confidence: 99%

Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release

Lee

Kang

et al. 2020

IJMS

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“…Perioperative acute hypoxic-ischemic cardiac toxicity of anesthetics is one of the most serious complications during surgical procedures, and occurs following the blockade of sodium channels and negative inotropic effect (1)(2)(3)(4). To avoid cardiac toxicity, selection of a suitable drug for the maintenance of anesthesia, especially during cardiac surgery, is crucial (5,6).…”

Section: Introductionmentioning

confidence: 99%

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

et al. 2020

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Propofol is a widely used intravenous anesthetic shown to exert a cardioprotective role against oxidative stress and ischemia/reperfusion injury in rat cardiac H9c2 cells. However, the regulatory mechanisms and functions of propofol in human cardiomyocytes remain unknown. The present study chemically induced hypoxia with cobalt chloride (CoCl 2 ) to mimic cardiomyocyte ischemic injury in human cardiac AC16 and HCM cells. To investigate its underlying mechanisms, propofol was added to the cells before the chemical hypoxia phase. The present results suggested that, in response to hypoxia, mitochondrial membrane potential was lost, and cardiomyocyte viability and superoxide dismutase levels decreased. However, the present results showed that reactive oxygen species and malondialdehyde levels increased. The present results suggested that these effects were significantly reversed following propofol treatment. Additionally, the present results suggested that the protective effect of propofol against CoCl 2 -induced injury may be inhibited by the activation of the JNK signaling pathways. The present results indicated that propofol pre-treatment inhibited CoCl 2 -induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders.

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“…Compared to other encapsulating carriers, liposomes may possess additional advantages when delivering LAs. As known by all, lipid emulsion therapy has shown its efficacy in dealing with systemic toxicity of LAs and been added into resuscitation guideline of LAs' toxicity [50]. The potential mechanisms include releasing LAs from Na v channels in myocardial cells, partitioning and redistributing LAs to storage (fatty acid), detoxification (liver) and excretion organs (kidney), providing extra energy, and augmenting Ca channels to strengthen cardiac output [51,52].…”

Section: Additional Advantagementioning

confidence: 99%

Advances of Nano-Structured Extended-Release Local Anesthetics

Qin

Huang

et al. 2020

Nanoscale Res Lett

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Extended-release local anesthetics (LAs) have drawn increasing attention with their promising role in improving analgesia and reducing adverse events of LAs. Nano-structured carriers such as liposomes and polymersomes optimally meet the demands of/for extended-release, and have been utilized in drug delivery over decades and showed satisfactory results with extended-release. Based on mature technology of liposomes, EXPAREL, the first approved liposomal LA loaded with bupivacaine, has seen its success in an extended-release form. At the same time, polymersomes has advances over liposomes with complementary profiles, which inspires the emergence of hybrid carriers. This article summarized the recent research successes on nano-structured extended-release LAs, of which liposomal and polymeric are mainstream systems. Furthermore, with continual optimization, drug delivery systems carry properties beyond simple transportation, such as specificity and responsiveness. In the near future, we may achieve targeted delivery and controlled-release properties to satisfy various analgesic requirements.

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Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity

Cited by 83 publications

References 108 publications

Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release

Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

Advances of Nano-Structured Extended-Release Local Anesthetics

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