Inhibition of Human Leukocyte Metabolism and Random Mobility by Local Anaesthesia

Hammer, Richard; Dahlgren, Cláes; Stendahl, Olle

doi:10.1111/j.1399-6576.1985.tb02246.x

Cited by 75 publications

(17 citation statements)

References 16 publications

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“…Since both a adrenergic and a petidergic hyperinnervation have been observed in patients with UC, neuro-immune interactions might contribute to the pathology in this disease [22][23][24]. Second, basal cell functions like collagen synthesis [3], cell motility [4][5][6] and cell metabolism [4,7] are affected by local anaesthetics. Furthermore, functions related to inflammation and immune response have also been described as being modified by local anaesthetic action, i.e.…”

Section: Introductionmentioning

confidence: 99%

Ropivacaine and lidocaine inhibit proliferation of non-transformed cultured adult human fibroblasts, endothelial cells and keratinocytes

Martinsson¹,

Hægerstrand

Dalsgaard³

1993

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Local anaesthetics are known to affect a variety of cell functions, many of which are involved in the inflammatory response. Local anaesthetics have also been shown to influence cell proliferation. The aim of this study was to examine the effect of two local anaesthetics (ropivacaine and lidocaine) on cell proliferation of cultured human fibroblasts, vascular endothelial cells and epithelial cells, i.e. keratinocytes, as earlier studies have not included primary human cell types. Significant inhibition of fibroblast proliferation was observed with concentrations of 50 microM ropivacaine or 100 microM lidocaine in 1% newborn calf serum and 500 microM ropivacaine or lidocaine in 10% newborn calf serum. The proliferation of endothelial cells was significantly inhibited by 1 mM ropivacaine in 5% human serum and 500 microM ropivacaine or 100 microM lidocaine in 40% human serum. Significant inhibition was not obtained with lidocaine when these cells were cultured in 5% HS. Significant inhibition of keratinocytes was obtained with 100 microM ropivacaine and 500 microM lidocaine. The effective concentrations are within the range of therapeutical concentrations in vivo and there seems to be a general correlation between the local anaesthetic potency and the inhibiting effect on cell proliferation. This suggest a mechanism by which local anaesthetics may exhibit anti-hyperproliferative effects in clinical situations.

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Section: Introductionmentioning

confidence: 99%

Ropivacaine and lidocaine inhibit proliferation of non-transformed cultured adult human fibroblasts, endothelial cells and keratinocytes

Martinsson¹,

Hægerstrand

Dalsgaard³

1993

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“…On one hand, the sodium channel block suppresses the neuronal signals, while on the other hand local anesthetics are known to have properties that are not regarded as directly analgesic [13]. In effect, some experimental studies have shown that local anesthetics reduce inflammatory mediator release by the neutrophils, reducing adhesion of the latter to the endothelium, and reducing the formation of free oxygen radicals [14][15][16][17]. We consider the cause for the analgesic improvement obtained with the administration of local anesthetic in the surgical incision zone to be related to its anti-inflammatory effects, which may sensitize the nociceptive receptors and contribute to pain and hyperalgesia after the operation.…”

Section: Discussionmentioning

confidence: 99%

Thoracic paravertebral block after thoracotomy: comparison of three different approaches☆

Garutti

González-Aragoneses

Biencinto

et al. 2009

European Journal of Cardio-Thoracic Surgery

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“…18,36 Lidocaine has been shown to inhibit multiple inflammatory responses, including inhibition of leukotriene and interleukin-1a release from polymorphonuclear leukocytes (PMNs). 37 This produces morphologic changes that inhibit PMN adherence 38 and thereby reduce PMN delivery to sites of inflammation, inhibit PMN migration and accumulation at sites of inflammation, 24,39,40 and block the priming of neutrophils, a potentiation response to several agents that has been implicated in the overstimulation of inflammatory pathways leading to undesirable damage to host tissue. 20,41 While the effects of local anesthetics on neutrophils and macrophages have been previously characterized, we present a novel finding of an attenuation in platelet-monocyte conjugates in cardiac surgical patients.…”

Section: Discussionmentioning

confidence: 99%

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

Klinger

Cooter

Berger

et al. 2016

Can J Anesth/J Can Anesth

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Purpose 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 intravenous lidocaine would attenuate the cerebral inflammatory response to cardiopulmonary bypass (CPB) by reducing the transcerebral activation gradients of platelets, leukocytes, and/or platelet-leukocyte conjugates. Methods We studied 202 patients undergoing cardiac surgery with CPB in this prospective randomized doubleblinded placebo-controlled trial. Subjects were randomized to receive either intravenous lidocaine (bolus ? 48-hr infusion) or placebo (identical infusion volume and duration). Paired jugular venous and radial arterial blood samples were drawn at several time points and analyzed by fluorescence-activated cell sorting to identify activated platelets and plateletleukocyte conjugates. Transcerebral activation gradients were calculated by subtracting arterial values from venous values and were compared between groups using repeated measures regression models with covariate adjustment for age, sex, surgery type, and CPB duration. Results Beginning after aortic cross-clamp release and peaking ten minutes after the termination of CPB, the mean (SD) transcerebral activation gradient of platelet-monocyte conjugates decreased in lidocaine-treated vs placebo-treated patients [-1.84 (11.47) mean linear fluorescence intensity (MLFI) vs 1.46 (13.88) MLFI, respectively; mean difference, -4.08 MLFI; 95% confidence interval, -7.86 to -0.29; P = 0.03). No difference was seen at any time point for activated platelets or for platelet-neutrophil conjugates. Conclusion While lidocaine did not affect the systemic or transcerebral activation of platelets or leukocytes, we did observe a reduction in the transcerebral activation of platelet-monocyte conjugates after aortic cross-clamp release. This may be a manifestation of reduced cerebral inflammation during cardiopulmonary bypass in response to treatment with lidocaine. This trial was registered at ClinicalTrials.gov (NCT00938964). RésuméObjectif Le dysfonctionnement cognitif postopératoire (DCPO) constitue une complication fréquente après une A list of all members of the Neurologic Outcome Research Group is given in the Appendix.

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Inhibition of Human Leukocyte Metabolism and Random Mobility by Local Anaesthesia

Cited by 75 publications

References 16 publications

Ropivacaine and lidocaine inhibit proliferation of non-transformed cultured adult human fibroblasts, endothelial cells and keratinocytes

Ropivacaine and lidocaine inhibit proliferation of non-transformed cultured adult human fibroblasts, endothelial cells and keratinocytes

Thoracic paravertebral block after thoracotomy: comparison of three different approaches☆

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

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