lidocaine/inflammation

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Effect of intravenous lidocaine on the transcerebral inflammatory response during cardiac surgery: a randomized-controlled trial.

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OBJECTIVE Postoperative cognitive dysfunction (POCD) occurs frequently after cardiac surgery. The pathophysiology of POCD remains elusive, but previous work showed that intravenous lidocaine may be protective against POCD, possibly by modulating cerebral inflammation. We hypothesized that

Lidocaine suppresses the increased extracellular signal-regulated kinase/cyclic AMP response element-binding protein pathway and pro-inflammatory cytokines in a neuropathic pain model of rats.

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OBJECTIVE Rats which have undergone spinal nerve ligation (SNL) display increases in the expression of extracellular signal-regulated kinase (ERK 1/2) and cyclic AMP response element-binding (CREB) protein. The present study was designed to determine whether lidocaine has a beneficial effect on the

Two for one: cyclic AMP mediates the anti-inflammatory and anti-spasmodic properties of the non-anesthetic lidocaine analog JMF2-1.

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Inhalation of JMF2-1, an analog of lidocaine with reduced anesthetic activity, prevents airway contraction and lung inflammation in experimental asthma models. We sought to test if the JMF2-1 effects are a consequence of increased intracellular cAMP levels in asthma cell targets, such as smooth

Lidocaine increases the anti-inflammatory cytokine IL-10 following mechanical ventilation in healthy mice.

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BACKGROUND Mechanical ventilation (MV) induces an inflammatory response that may result in (acute) lung injury. Lidocaine, an amide local anesthetic, has anti-inflammatory properties in vitro and in vivo, possibly due to an attenuation of pro-inflammatory cytokines, intracellular adhesion molecule-1

Inhibition of the neurogenic inflammatory response by lidocaine in rat skin.

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Axon reflex vasodilatation and neurogenic plasma extravasation are characteristic cutaneous vascular responses mediated by neuropeptides released from stimulated capsaicin-sensitive sensory nerve endings. Intracutaneous injections of local anaesthetics inhibit the axon-reflex flare elicited by

Comparison of liposomal and 2-hydroxypropyl-β-cyclodextrin-lidocaine on cell viability and inflammatory response in human keratinocytes and gingival fibroblasts.

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OBJECTIVE The aim of this study was to observe the effect multilamellar liposomes (MLV) and 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) in the in-vitro effects of lidocaine in cell viability, pro-inflammatory cytokines and prostaglandin E2 release of both human keratinocytes (HaCaT) and gingival

Absence of cytotoxic and inflammatory effects following in vitro exposure of chondrogenically-differentiated human mesenchymal stem cells to adenosine, lidocaine and Mg2+ solution.

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BACKGROUND

ALM solution, a combination of adenosine, lidocaine and Mg²⁺, is an emerging small volume therapy that has been shown to prevent and correct coagulopathy and surgery-related inflammation in preclinical models, though its application in orthopaedic surgery is

Small-bowel obstruction and the effects of lidocaine, atropine and hexamethonium on inflammation and fluid losses.

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BACKGROUND The profuse fluid losses and morbidity of patients suffering from obstructive ileus are closely related to inflammatory changes in the obstructed bowel wall. Previous experimental studies have shown that use of steroids and NSAIDs can reduce fluid losses in obstructive ileus. In the

C-fiber spontaneous discharge evoked by chronic inflammation is suppressed by a long-term infusion of lidocaine yielding nanogram per milliliter plasma levels.

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Nociceptors innervating inflamed tissue acquire an abnormal spontaneous discharge that is believed to be at least part of the reason for the persistent spontaneous pain, allodynia, and hyperalgesia that accompany inflammation. Recent studies suggest that patients with chronic inflammatory pain may

Effect of inflammation on the metabolism of antipyrine, lidocaine and propranolol in isolated rat hepatocytes.

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A decrease of the hepatic intrinsic clearance could contribute to the increase of the plasma concentrations of alpha 1-acid glycoprotein-bound drugs such as propranolol in animals and humans with inflammation. Therefore, the influence of inflammation upon the metabolism of propranolol and another

Dysfunctional phagocytosis capacity, granulocyte recruitment and inflammatory factor secretion of Kupffer cells in diabetes mellitus reversed by Lidocaine.

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Kupffer cells (KCs) present dysfunctional immunity capacity among the diabetes mellitus patients. This study aims to investigate whether Lidocaine could reverse dysfunctions of KCs, in terms of phagocytosis, granulocyte recruitment and inflammatory mediator

Relationship between inflammation, alpha-1-acid glycoprotein and lidocaine tolerance during fiber-optic bronchoscopy.

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The purpose of this study was to determine the relationship between inflammation, increased alpha-1-acid glycoprotein (AAG), and lidocaine tolerance during fiber-optic bronchoscopy. Previous studies indicate that serum lidocaine levels vary widely from one individual to another. One reason for these

Lidocaine attenuates the hypotensive and inflammatory responses to endotoxemia in rabbits.

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OBJECTIVE To assess the effects of lidocaine on the hemodynamic and inflammatory responses to Escherichia coli endotoxemia in rabbits. METHODS Prospective, randomized, controlled experimental study. METHODS University laboratory. METHODS Twenty-seven female Japanese rabbits, anesthetized with

Treatment of lidocaine on subacute thyroiditis via restraining inflammatory factor expression and inhibiting pyroptosis pathway.

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To explore the role of lidocaine on subacute thyroiditis (SAT) and the molecular mechanism.SAT models were constructed by infecting adenovirus to thyroid follicular epithelial cells. Cells were randomly divided into five groups: model group, low lidocaine,

[Influence of lidocaine on systemic inflammation in perioperative patients undergoing cardiopulmonary bypass].

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OBJECTIVE To investigate the influence of lidocaine on systemic inflammation in the perioperative ventricular septal defect (VSD). METHODS Twenty patients, scheduled for ventricular septal defect were randomly divided into 2 groups: lidocaine and control groups. Before rebeat lidocaine 1 mg/kg was

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