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Endothelial barrier protection by local anesthetics: ropivacaine and lidocaine block tumor necrosis factor-α-induced endothelial cell Src activation.
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BACKGROUND
Pulmonary endothelial barrier dysfunction mediated in part by Src-kinase activation plays a crucial role in acute inflammatory disease. Proinflammatory cytokines, such as tumor necrosis factor-α (TNFα), activate Src via phosphatidylinositide 3-kinase/Akt-dependent nitric oxide generation,
Effects of lidocaine and droxicainide on myocardial necrosis: a comparative study.
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Lidocaine has been shown to protect ischemic myocardium, but the degree of its effectiveness is not yet well established. Therefore, in this study, the effects of this drug on ultimate infarct size were examined quantitatively. Another member of the same class of drugs, droxicainide (ALS1249),
Clinical dose of lidocaine destroys the cell membrane and induces both necrosis and apoptosis in an identified Lymnaea neuron.
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OBJECTIVE
Although lidocaine-induced cell toxicity has been reported, its mechanism is unclear. Cell size, morphological change, and membrane resistance are related to homeostasis and damage to the cell membrane; however, the effects of lidocaine on these factors are unclear. Using an identified
Prolonged perivascular use of verapamil or lidocaine decreases skin flap necrosis.
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During this experiment the authors investigated whether prolonged local use of verapamil or lidocaine prevents vasoconstriction and establishes better blood supply to the rat epigastric skin flap, hence reducing the necrosis that occurs otherwise. Abdominal wall skin flaps of 45 Sprague-Dawley rats,
Mechanism of epinephrine enhancement of lidocaine-induced skeletal muscle necrosis.
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Epinephrine significantly increases lidocaine-induced skeletal muscle necrosis, even in low concentrations that elicit no damage by themselves. Inasmuch as isoproterenol had no influence on lidocaine myotoxicity, a direct effect of epinephrine on muscle fibers is unlikely. Two vasoconstrictors with
[Eyelid necrosis after injection of lidocaine with epinephrine].
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Four patients (two women aged 50 and 67 years, a 36-year-old man, and a 5-year-old child) presented with necrosis of the eyelid after local anesthesia using 2% lidocaine with epinephrine. In three cases, the anesthesia was administered prior to suturing an eyelid laceration, and the necrosis
Intravenous lidocaine decreases tumor necrosis factor alpha expression both locally and systemically in pigs undergoing lung resection surgery.
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BACKGROUND
Lung resection surgery is associated with an inflammatory reaction. The use of 1-lung ventilation (OLV) seems to increase the likelihood of this reaction. Different prophylactic and therapeutic measures have been investigated to prevent lung injury secondary to OLV. Lidocaine, a commonly
Digital Necrosis After Lidocaine and Epinephrine Injection in the Flexor Tendon Sheath Without Phentolamine Rescue.
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The literature generally supports the safety of epinephrine injection in the digits, but recent case reports describe ischemic adverse events associated with the use of lidocaine and epinephrine in which phentolamine rescue was not performed. We present a case of finger necrosis and subsequent
Lidocaine-induced apoptosis and necrosis in U937 cells depending on its dosage.
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Local anesthetics are known to affect a variety of cellular responses other than the action of anesthetics through the Na(+) channel blockade. In this study, we examined the effect of a common local anesthetic lidocaine on the cellular activity and viability of human histiocytic lymphoma U937 cells.
Decreased incidence of acute tubular necrosis after cadaveric donor transplantation due to lidocaine donor pretreatment and low-dose dopamine infusion in the recipient.
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Lidocaine, 2-chlorprocaine and hepatic necrosis.
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Necrosis of the eyebrow after local injection of lidocaine 2% on the lower eyelid: is a thrombus-embolic mechanism involved?
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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
Protective effect of lidocaine in the experimental foot-and-mouth disease pancreatitis.
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Experimental infection of mice with foot-and-mouth disease virus (FMDV) induces a necrotizing pancreatitis of the exocrinar portion of the organ. The lesions are characterized by vascular congestion, edema and interstitial polymorphonuclear leukocyte (PMN) infiltrates. When infected mice were
The antioxidant N-acetyl cysteine suppresses lidocaine-induced intracellular reactive oxygen species production and cell death in neuronal SH-SY5Y cells.
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The local anesthetic lidocaine can affect intra- and extra-cellular signaling pathways in both neuronal and non-neuronal cells, resulting in long-term modulation of biological functions, including cell growth and death. Indeed, lidocaine was shown to induce necrosis and apoptosis in vitro. While
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