Different effects of local anesthetics on calcium influx into rat mast cells

Ohishi, Kazuhiko; Suzuki, Tamiko; Uchida, Masaatsu K.

doi:10.1016/0306-3623(85)90069-2

Cited by 9 publications

(4 citation statements)

References 13 publications

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“…Thus, the effects of lidocaine on the histamine release induced by polycations are similar to that on the release induced by compound 48/ 80. One of the mechanisms for the inhibitory effect of lidocaine on histamine release in duced by Con A was due to inhibition of calcium influx into mast cells (14). However, lidocaine inhibits the histamine release in duced by calcium ionophore A23187 when there is enough intracellular calcium to trigger histamine releases, suggesting that their in hibitory actions on histamine release induced by A.23187 cannot be explained by their effect on calcium influx (14).…”

Section: Discussionmentioning

confidence: 99%

“…One of the mechanisms for the inhibitory effect of lidocaine on histamine release in duced by Con A was due to inhibition of calcium influx into mast cells (14). However, lidocaine inhibits the histamine release in duced by calcium ionophore A23187 when there is enough intracellular calcium to trigger histamine releases, suggesting that their in hibitory actions on histamine release induced by A.23187 cannot be explained by their effect on calcium influx (14). Our group previously reported that the inhibitory effects of lidocaine on mast cells was correlated with the concen tration of nonionized molecules which pene trate the mast cell membrane (10).…”

Section: Discussionmentioning

confidence: 99%

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Comparison of histamine release induced by synthetic polycations with that by compound 48/80 from rat mast cells.

et al. 1990

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Abstract-We compared the histamine release induced by polyethylenimines and polyallylamines with that induced by compound 48/80.Lidocaine inhibited the histamine release induced by polyethylenimine with a molecular weight of 600 (PEI6), but disodium cromoglycate did not. The histamine releases induced by all polyethylenimines and polyallylamines tested were inhibited by lidocaine, but not by disodium cromoglycate.islet activating protein inhibited the histamine release induced by PEI6. Its effects on the release by other polyethylenimines and polyallylamines were less than that on PEI6. It is likely that the inhibition of G proteins by islet activating protein resulted in a decrease of the histamine release. This possibility was supported by the finding that guanyl-5'-(8,r-imino) triphos phate enhanced the histamine release.An inhibitor of polyphosphoinositide phos phodiesterase, neomycin, did not affect the histamine releases induced by these polymers.The effect of PEI6 seemed to resemble that of compound 48/80. After pretreatment of mast cells with wheat germ agglutinin and with Limax flavus ag glutinin, releases of histamine induced by PEI6 and compound 48/80 decreased, suggesting that the binding sites of PEI6 and compound 48/80 had sialic acid and/ or N-acetyl glucosamine residues. The binding site for PEI6 seemed to especially overlap those of compound 48/80.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Comparison of histamine release induced by synthetic polycations with that by compound 48/80 from rat mast cells.

et al. 1990

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“…The increase of [Ca 2ϩ ] i is an important response after cytokine stimulation. Lidocaine was reported to inhibit [Ca 2ϩ ] i accumulation and decrease calcium influx in mast cells (24). In this study, lidocaine inhibited MCP-1 stimulated calcium influx in THP-1 cells.…”

Section: Discussionmentioning

confidence: 87%

Lidocaine Attenuates Monocyte Chemoattractant Protein-1 Production and Chemotaxis in Human Monocytes: Possible Mechanisms for Its Effect on Inflammation

Li¹,

Tsai²,

Hsu³

et al. 2003

Anesthesia & Analgesia

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“…Similarly, Sasagawa et al [ 28 ] described the inhibitory effect of lidocaine on the chemotaxis of neutrophils. One of the proposed mechanisms that explain this effect is the inhibition by lidocaine of the accumulation of calcium and a subsequent decrease in the influx of this ion in mast cells [ 29 ]. This suggests that it is capable of suppressing the monocytic activation triggered by MCP-1 in the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

Effect of Intravenous Lidocaine on Inflammatory and Apoptotic Response of Ischemia-Reperfusion Injury in Pigs Undergoing Lung Resection Surgery

Romera

Cebollero

Romero-Gómez

et al. 2021

BioMed Research International

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Background. Ischemia-reperfusion injury is one of the most critical phenomena in lung transplantation and causes primary graft failure. Its pathophysiology remains incompletely understood, although the inflammatory response and apoptosis play key roles. Lidocaine has anti-inflammatory properties. The aim of this research is to evaluate the effect of intravenous lidocaine on the inflammatory and apoptotic responses in lung ischemia-reperfusion injury. Methods. We studied the histological and immunohistochemical changes in an experimental model of lung transplantation in pigs. Twelve pigs underwent left pneumonectomy, cranial lobectomy, caudal lobe reimplantation, and 60 minutes of graft reperfusion. Six of the pigs made up the control group, while six other pigs received 1.5 mg/kg of intravenous lidocaine after induction and a 1.5 mg/kg/h intravenous lidocaine infusion during surgery. In addition, six more pigs underwent simulated surgery. Lung biopsies were collected from the left caudal lobe 60 minutes after reperfusion. We conducted a double study on these biopsies and assessed the degree of inflammation, predominant cell type (monocyte-macrophage, lymphocytes, or polymorphous), the degree of congestion, and tissue edema by hematoxylin and eosin stain. We also conducted an immunohistochemical analysis with antibodies against CD68 antigens, monocyte chemoattractant protein-1 (MCP-1), Bcl-2, and caspase-9. Results. The lungs subjected to ischemia-reperfusion injury exhibited a higher degree of inflammatory infiltration. The predominant cell type was monocyte-macrophage cells. Both findings were mitigated by intravenous lidocaine administration. Immunohistochemical detection of anti-CD68 and anti-MCP-1 showed higher infiltration in the lungs subjected to ischemia-reperfusion injury, while intravenous lidocaine decreased the expression. Ischemia-reperfusion induced apoptotic changes and decreased Bcl-2 expression. The group treated with lidocaine showed an increased number of Bcl-2-positive cells. No differences were observed in caspase-9 expression. Conclusions. In our animal model, intravenous lidocaine was associated with an attenuation of the histological markers of lung damage in the early stages of reperfusion.

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Different effects of local anesthetics on calcium influx into rat mast cells

Cited by 9 publications

References 13 publications

Comparison of histamine release induced by synthetic polycations with that by compound 48/80 from rat mast cells.

Comparison of histamine release induced by synthetic polycations with that by compound 48/80 from rat mast cells.

Lidocaine Attenuates Monocyte Chemoattractant Protein-1 Production and Chemotaxis in Human Monocytes: Possible Mechanisms for Its Effect on Inflammation

Effect of Intravenous Lidocaine on Inflammatory and Apoptotic Response of Ischemia-Reperfusion Injury in Pigs Undergoing Lung Resection Surgery

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