Use of lidocaine by continuous infusion

Bassan, Mayer; Weinstein, Steven R.; Mandel, William J.

doi:10.1016/0002-8703(74)90069-6

Cited by 21 publications

(7 citation statements)

References 5 publications

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“…Furthermore, although we did not measure plasma lidocaine concentration in chronic lidocaine-exposed mice, systemic toxicities of lidocaine were not observed in any mice. Previous study by Bassan et al25 showed that the plasma concentration of lidocaine reaches 2-6.5 μg/ml after 1 mg/kg initial dose and subsequent 2-3 mg/min continuous intravenous administration in human adult. In this setting, the total dose of lidocaine is 2,950-4,390 mg/day for a 70-kg human.…”

Section: Discussionmentioning

confidence: 95%

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Lidocaine suppresses mouse Peyer's Patch T cell functions and induces bacterial translocation

Kawasaki

Sata

et al. 2011

Surgery

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The gastrointestinal mucosa is an important route of entry for microbial pathogens. The immune cells of Peyer's patch (PP) compartments contribute to the active immune response against infection. Although local anesthetics are widely used in clinical practice, it remains unclear whether local anesthetics such as lidocaine affect PP T cell functions. The aim of this study was to examine if lidocaine has any effects on mouse PP T cell functions. To test this, freshly isolated mouse Peyer's patch T cells were incubated with lidocaine. The effects of lidocaine on concanavalin A-stimulated PP T cell proliferation and cytokine production were assessed. The effect of lidocaine on PP T cell mitogen-activated protein kinase (MAPK) activation was also assessed. The results indicate that lidocaine suppresses cell proliferation, cytokine production, and MAPK activation in PP T cells. Furthermore, we found that the chronic in vivo exposure to lidocaine increases bacterial accumulation in PP. The enhanced immunosuppressive effects of lidocaine on PP T cell functions could contribute to the host's enhanced susceptibility to infection.

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Section: Discussionmentioning

confidence: 95%

“…Previously, Wu et al25 demonstrated that intestinal IgA levels are correlated with intestinal Th2 cytokine concentration. They found intravenous total parenteral nutrition decreases production of Th2 cytokines and induces severely impaired mucosal immunity.…”

Section: Discussionmentioning

confidence: 99%

Lidocaine suppresses mouse Peyer's Patch T cell functions and induces bacterial translocation

Kawasaki

Sata

et al. 2011

Surgery

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“…Other workers have observed a fall in plasma concentrations below therapeutic levels when a single bolus injection is followed by an infusion of 2 to 3 mg/minute (Bassan et al, 1974;Greenblatt et al, 1976). Low plasma concentrations of lignocaine may be hazardous.…”

Section: Discussionmentioning

confidence: 99%

Observations on intravenous administration of lignocaine in patients with myocardial infarction.

Campbell¹,

Kelly²,

Adgey³

et al. 1978

Heart

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suMMARY Lignocaine was administered intravenously to 36 patients with acute myocardial infarction.A bolus of 100 mg followed by an infusion of 2 mg/minute failed to maintain plasma levels above 2 ,g/ml. A bolus of 100 mg followed by 4 mg/minute also failed to maintain satisfactory plasma concentrations during the first hour of therapy.A bolus of 75 mg was combined with an infusion of 10 mg/minute for 20 minutes followed by 1.5 mg/ minute. Satisfactory plasma concentrations during the first hour were observed in 94 per cent of the estimations. No important adverse side effects occurred during the infusion of 10 mg/minute.Lignocaine has been found to be relatively ineffective in controlling ventricular arrhythmias occurring immediately after the onset of acute myocardial infarction (Geddes et al., 1972). This may be related in some cases to the presence of sympathetic overactivity in the acute phase of myocardial infarction since the drug has been shown to be more effective when the heart rate is within the normal range (Pantridge et al., 1974). However, failure to achieve adequate plasma concentrations may be an important reason for therapeutic ineffectiveness. It has been said that plasma concentrations of lignocaine of 2 to 5 ,ug/ml are usually effective (Koch-Weser, 1972). In this study, the plasma concentrations of lignocaine obtained with conventional doses of the drug have been investigated.We have used a theoretical approach to design a regimen that might give therapeutic plasma concentrations, particularly throughout the first hour of therapy. Patients and methodsThirty-six patients were studied (Table 1). All received lignocaine because of ventricular arrhythmias complicating acute myocardial infarction. Six had self-terminating ventricular tachycardia. The remainder had ventricular extrasystoles (frequent, consecutive, or R on T). The drug was given to-all patients within 48 hours of the onset of symptoms Received for publication 9 January 1978 of infarction (median 10 hours). Twenty-six (72%) of the patients had clinical or radiographic evidence of left ventricular failure when treatment was started. None had pulmonary oedema or cardiogenic shock.The 36 patients were divided into 4 groups. Group 1 (10 patients) received an initial 100 mg injection of lignocaine over 30 seconds. This was followed immediately by a continuous infusion of the drug at a rate of 2 mg/minute. Groups 2 and 3 (each containing 10 patients) also received an initial 100 mg injection but this was followed by a 4 mg/ minute infusion for 20 and 45 minutes, respectively. The rate of infusion was then reduced to 2 mg/ minute. Group 4 (6 patients) received an initial 75 mg injection of lignocaine given over 30 seconds followed by a 10 mg/minute infusion for 20 minutes. The infusion rate was then reduced to 1-5 mg/ minute. The regimen in Group 4 was devised using the method of Wagner (1974). Wagner suggested that a drug might be given intravenously using 2 different infusion rates-an initial rapid rate (Q1) and a later slower rate (Q2). ...

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“…However, results from our own institution (Bassan et al, 1974) show that using the standard combined 1 mg/kg initial bolus and weight-related constant infusion, a significant drop in plasma levels to less than 90 per cent of peak serum concentrations will occur 20 to 30 minutes after starting the infusion. Moreover, peak steady state levels are not achieved until at least 6 hours after onset of infusion (Bassan et al, 1974).…”

Section: Conventional Lignocaine Administration Includesmentioning

confidence: 90%

“…Moreover, peak steady state levels are not achieved until at least 6 hours after onset of infusion (Bassan et al, 1974). The therapeutic dilemma is, therefore, to maintain adequate serum levels while the bolus is rapidly being degraded and the constant infusion is slowly increasing serum levels.…”

Section: Conventional Lignocaine Administration Includesmentioning

confidence: 99%

Lignocaine: a new technique for intravenous administration.

Levy¹,

Charuzi²,

Mandel³

1977

Heart

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Current practices of intravenous lignocaine administration may result in a significant drop in blood level between the peak serum level from the initial bolus and the subsequent steady state from the constant infusion. This can cause a significant interval when plasma lignocaine levels are less than therapeutic, and ventricular ectopy may occur. To eliminate this subtherapeutic interval, a new therapeutic approach was devised. Seven patients were studied who had no evidence of congestive heart failure or liver disease. Lignocaine was infused at a rate of 25 mg/min; infusion dosages were selected by patient weight. The above therapeutic regimen eliminated the subtherapeutic hiatus and did not result in clinical toxicity. Therefore, this new infusion technique has significant clinical advantages in patients who require therapy with intravenous lignocaine.

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Use of lidocaine by continuous infusion

Cited by 21 publications

References 5 publications

Lidocaine suppresses mouse Peyer's Patch T cell functions and induces bacterial translocation

Lidocaine suppresses mouse Peyer's Patch T cell functions and induces bacterial translocation

Observations on intravenous administration of lignocaine in patients with myocardial infarction.

Lignocaine: a new technique for intravenous administration.

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