The effect of lidocaine on neutrophil CD11b/CD18 and endothelial ICAM-1 expression and IL-1β concentrations induced by hypoxia–reoxygenation

Lan, Wei; Harmon, Dominic; Wang, J. H.; Shorten, George; Redmond, Paul

doi:10.1017/s0265021504000353

Cited by 19 publications

(22 citation statements)

References 21 publications

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“…IL-1 also activates production of other cytokines, such as IL-6, IL-8 and TNF [2]. Several reports have suggested that Lid has anti-inflammatory action, such as suppression of proinflammatory cytokine production [15], suppression of histamine release from basophiles and mast cells [31], attenuation of monocyte chemoattractant protein-1 production and reduction of chemotaxis [17]. Therefore, our results suggest that Lid might be useful not only as a local anesthetic but also as an anti-inflammatory drug in cows.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Lidocaine Hydrochloride on the Function of Bovine Peripheral Leukocytes

Ando

Ogawa

Fujiwara

et al. 2009

The Journal of Veterinary Medical Science

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ABSTRACT. To clarify the effect of lidocaine hydrochloride (Lid) on bovine peripheral granulocyte phagocytosis, adhesion molecule expression of leukocytes and peripheral blood mononuclear cell mRNA expression of cytokines were investigated. Lid was added to blood samples at a final concentration of 0 (only PBS; Cont), 0.2 mg/ml or 2.0 mg/ml. Phagocytosis of granulocytes was significantly decreased by addition of 2.0 mg/ml of Lid. CD18 expression of granulocytes and mononuclear cells were significantly reduced by addition of 2.0 mg/ml of Lid. IL-1 and IL-8 mRNA expressions of mononuclear cells were also significantly reduced by addition of 2.0 mg/ml of Lid other hand. These results suggest that Lid might reduce the protective immunity of cows. On the other hand, reduction of CD18, IL-1 and IL-8 mRNA expression also indicates that Lid has an anti-inflammatory effect in cows. KEY WORDS: adhesion molecules, anti-inflammatory effect, cattle, lidocaine hydrochloride, phagocytosis.

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Section: Discussionmentioning

confidence: 99%

“…Several reports suggested that LAs reduce the phagocytosis, chemotaxis, adhesion molecule expression, and production of superoxides of granulocytes [11,13,15,24]. It has also been reported that LAs reduce the lymphocyte blast transformation and cytokine secretion of mononuclear cells [6,25,29].…”

mentioning

confidence: 99%

Effect of Lidocaine Hydrochloride on the Function of Bovine Peripheral Leukocytes

Ando

Ogawa

Fujiwara

et al. 2009

The Journal of Veterinary Medical Science

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“…In addition, lidocaine can reduce the expression of endothelial adhesion molecules in epithelial cells, endothelial cells and neutrophils and could thereby inhibit neutrophil adhesion and migration (Lan et al 2004). In rats with experimentally induced obstructive ileus, IV administration of lidocaine prevents fluid secretion into the lumen of the small intestine and reduces edema formation in the intestinal wall (Nellgard et al 1996).…”

Section: Lidocainementioning

confidence: 99%

Ischemia in equine intestine – mechanisms of injury and methods of treatment

Freeman¹,

Grosche²

2012

PHK

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SummaryThe importance of reperfusion injury in equine intestine is controversial and unclear. Large colon volvulus and small intestinal strangulation are the most devastating causes of intestinal ischemia in horses and result in severe mucosal damage, barrier dysfunction, endotoxic shock and death. Although essential for tissue recovery, reperfusion after these types of ischemia could exacerbate intestinal injury. Responses to ischemia and reperfusion (I/R) involve a series of synchronized biochemical, cellular and structural changes characterized by generation of reactive oxygen metabolites, activation of immune cells, and epithelial cell degeneration and death. The intensity of neutrophil activation and influx is central to the process of reperfusion injury and the associated inflammatory events. The classic paradigm of reperfusion injury is best displayed after the segmental hypoperfusion or low-flow ischemia model, in which arterial inflow is adjusted to 20% of normal baseline flow, and then allowed to return to normal or greater values during reperfusion. In such cases, injury during the ischemic phase is mild, compared with the reperfusion injury that follows. Although there is some evidence of reperfusion injury in equine colon and jejunum after low-flow ischemia, attempts to ameliorate this by pharmacologic means have met with only moderate success. A multimodal approach, using solutions designed to improve survival in transplanted organs, seems to hold the greatest promise, although these have not been embraced in the clinical setting. Expense and difficulties in delivery are the two most serious limitations. Recent studies to assess the effect of colonic I/R on equine pelvic flexure involved a complete ischemia model that was similar to the clinical lesion, and for periods of 1 to 2 hours of ischemia followed by 30 minutes, 4 hours, or 18 hours of reperfusion. Ischemia caused degeneration and detachment of epithelial cells, early apoptosis, and opening of tight junctions (TJs), all of which decreased transepithelial resistance (TER) and increased mannitol flux when the tissues were studied in vitro. Autophagy was a prominent feature in epithelial cells after 1 hour of ischemia. Reperfusion was characterized by apoptosis, epithelial regeneration, and closure of TJs with improved TER and reduced mannitol leakage. Neutrophils infiltrated colonic mucosa during reperfusion, and macrophages, mast cells and eosinophils were activated during I/R. Equine colonic mucosa subjected to ischemia can repair rapidly and regain barrier integrity during reperfusion, despite intense mucosal inflammation. Recently, attention has focused on inflammation induced by intestinal handling and on remote organ responses to intestinal injury, both of which could be highly relevent to postoperative management of horses that undergo colic surgery. The use of lidocaine in a continuous rate infusion is a popular approach to ameliorate the intestinal inflammatory response after colic surgery, although there is no evidence that it has a...

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“…These include interactions with and alterations of functions in host neutrophils and macrophages. For instance, lidocaine was found to affect functions such as chemotaxis, phagocytosis, superoxide anion and lysosomal enzyme release as well as pro-and anti-inflammatory cytokines production by neutrophils [9][10][11] . Similarly, the anti-inflammatory properties of lidocaine have been shown to be effective in the treatment of LPS-induced ALI.…”

Section: Introductionmentioning

confidence: 99%

Lidocaine Attenuates Lipopolysaccharide-Induced Acute Lung Injury through Inhibiting NF-κB Activation

et al. 2007

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Background and Objectives: Lidocaine has been reported to attenuate the inflammatory response in addition to its anesthetic activity, but the mechanisms are poorly understood. The objective of this study is to determine if lidocaine prior to endotoxemia diminishes pulmonary dysfunction by blocking the NF-ĸB activation. Methods: Rats were assigned to: (1) control (0.9% sodium chloride); (2) lipopolysaccharides (LPS); (3) LPS + lidocaine 1 mg/kg; (4) LPS + lidocaine 2 mg/kg, and (5) LPS + lidocaine 4 mg/kg. The LPS and LPS + lidocaine 4 mg/kg groups were subjected to 1-, 3-, 6- and 12-hour time points. To investigate the activation of NF-ĸB, the expression of NF-ĸB in the nuclear and IĸBα in the cytosol extracts were analyzed by Western blot. The concentration of TNF-α and IL-6 in serum was detected by ELISA. The pathologic changes of the lung were observed using HE staining. Results: After i.p. injection of LPS, the expression of NF-ĸB in the nuclear extracts was significantly increased and IĸBα in the cytosol extracts was markedly decreased. The concentration of TNF-α and IL-6 in serum was increased. Pathological examination showed that the normal structure of the lung was destroyed badly. However, lidocaine reversed the above results. Conclusion: Lidocaine attenuates LPS-induced lung injury via mechanisms involving inhibiting NF-ĸB activation and cytokine release, which implies that lidocaine may be a potential anti-inflammatory agent in endotoxemia.

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The effect of lidocaine on neutrophil CD11b/CD18 and endothelial ICAM-1 expression and IL-1β concentrations induced by hypoxia–reoxygenation

Abstract: Lidocaine at clinically relevant concentrations decreased neutrophil CD18 and endothelial ICAM-1 expression but not endothelial IL-1beta concentrations.

Cited by 19 publications

References 21 publications

Effect of Lidocaine Hydrochloride on the Function of Bovine Peripheral Leukocytes

Effect of Lidocaine Hydrochloride on the Function of Bovine Peripheral Leukocytes

Ischemia in equine intestine – mechanisms of injury and methods of treatment

Lidocaine Attenuates Lipopolysaccharide-Induced Acute Lung Injury through Inhibiting NF-κB Activation

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