Intravenous lignocaine anÆsthesia

Clive-Lowe, S.G. De; Desmond, J. W.; North, Judith

doi:10.1111/j.1365-2044.1958.tb08045.x

Cited by 69 publications

(36 citation statements)

References 2 publications

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“…For example, our findings with lidocaine, which has well-known general anesthetic properties (see Introduction), 1,3 share some noteworthy similarities with those recently obtained with propofol. 57 In thalamocortical neurons, propofol inhibited I h -HCN2 at clinically relevant concentrations (e.g., 36% at 5 M; 23°C) and slowed I h activation.…”

Section: H : An Emerging Anesthetic Drug Target In the Thalamus?supporting

confidence: 64%

“…It also is useful systemically in the management of acute postoperative and chronic neuropathic pain syndromes, in the maintenance of general anesthesia, and as a class IB antiarrhythmic. [1][2][3][4][5] In addition, systemic lidocaine exhibits concentration-dependent central nervous system (CNS) toxicity that begins with alterations in sensorium at low plasma concentrations that overlap with those associated with the therapeutic effects (in humans, typically less than 5 g/ml or approximately 20 M) and progresses to generalized seizures, coma, and death at higher levels (approximately Ͼ15-50 g/ml or 60 -200 M). 6,7 Though poorly understood, the mechanisms that underlie lidocaine's complex concentration-dependent supraspinal CNS effects are not solely explained by its classic action on Na ϩ channels.…”

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confidence: 99%

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Lidocaine Blocks the Hyperpolarization-activated Mixed Cation Current, I h, in Rat Thalamocortical Neurons

Putrenko

Schwarz

2011

Anesthesiology

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Background:The mechanisms that underlie the supraspinal central nervous system effects of systemic lidocaine are poorly understood and not solely explained by Na ϩ channel blockade. Among other potential targets is the hyperpolarization-activated cation current, I h , which is blocked by lidocaine in peripheral neurons. I h is highly expressed in the thalamus, a brain area previously implicated in lidocaine's systemic effects. The authors tested the hypothesis that lidocaine blocks I h in rat thalamocortical neurons. Methods:The authors conducted whole cell voltage-and current-clamp recordings in ventrobasal thalamocortical neurons in rat brain slices in vitro. Drugs were bath-applied. Data were analyzed with Student t tests and ANOVA as appropriate; ␣ ϭ 0.05. Results: Lidocaine voltage-independently blocked I h , with high efficacy and a half-maximal inhibitory concentration (IC 50 ) of 72 M. Lidocaine did not affect I h activation kinetics but delayed deactivation. The I h inhibition was accompanied by an increase in input resistance and membrane hyperpolarization (maximum, 8 mV). Lidocaine increased the latency of rebound low-threshold Ca 2ϩ spike bursts and reduced the number of action potentials in bursts. At depo-

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Section: H : An Emerging Anesthetic Drug Target In the Thalamus?supporting

confidence: 64%

mentioning

confidence: 99%

Lidocaine Blocks the Hyperpolarization-activated Mixed Cation Current, I h, in Rat Thalamocortical Neurons

Putrenko

Schwarz

2011

Anesthesiology

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“…They showed that lidocaine provides post-operative analgesia with low incidence of post-operative nausea and vomiting [13]. Other studies showed that the use of lignocaine with thiopentone nitrous oxide-oxygen provide post-operative analgesia, low incidence of nausea and vomiting, and short recovery time without changes in pulse rate or blood pressure [14,15]. In our study, we assessed the intraoperative analgesic effects of a constant IV infusion of lidocaine during lumbotomy in adult patients under general anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Intravenous lidocaine as adjuvant to general anesthesia in renal surgery

Nakhli

Kahloul

Guizani

et al. 2018

Libyan Journal of Medicine

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The role of intraoperative intravenous lidocaine infusion has been previously evaluated for pain relief, inflammatory response, and post-operative recovery, particularly in abdominal surgery. The present study is a randomized double-blinded trial in which we evaluated whether IV lidocaine infusion reduces isoflurane requirement, intraoperative remifentanil consumption and time to post-operative recovery in non-laparoscopic renal surgery. Sixty patients scheduled to undergo elective non-laparoscopic renal surgery under general anesthesia were enrolled to receive either systemic lidocaine infusion (group L: bolus 1.5 mg/kg followed by a continuous infusion at the rate of 2 mg/kg/hr until skin closure) or normal saline (0.9% NaCl solution) (Group C). The depth of anesthesia was monitored using the Bispectral Index Scale (BIS), which is based on measurement of the patient’s cerebral electrical activity. Primary outcome of the study was End-tidal of isoflurane concentration (Et-Iso) at BIS values of 40–60. Secondary outcomes include remifentanil consumption during the operation and time to extubation. Et-Iso was significantly lower in group L than in group C (0.63% ± 0.10% vs 0.92% ± 0.11%, p < 10–3). Mean remifentanil consumption of was significantly lower in group L than in group C (0.13 ± 0.04 µg/kg/min vs 0.18 ± 0.04 µg/kg/min, p < 10–3). Thus, IV lidocaine infusion permits a reduction of 31% in isoflurane concentration requirement and 27% in the intraoperative remifentanil need. In addition, recovery from anesthesia and extubation time was shorter in group L (5.8 ± 1.8 min vs 7.9 ± 2.0 min, p < 10–3). By reducing significantly isoflurane and remifentanil requirements during renal surgery, intravenous lidocaine could provide effective strategy to limit volatile agent and intraoperative opioids consumption especially in low and middle income countries.

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“…These include neoplastic pain (Cavallini & Beltrami, 1968), post-operative pain (McLachlin, 1945; Keats et al, 1951;De Clive-Lowe, 1958;Bartlett & Hutaserani, 1961;Nalda Felipe et al, 1977;De Gaudio et al, 1978;Marchisio, 1980), post-traumatic pain (Schnapp, 1981), neuralgic pain (Boas et al, 1982;Lindblom & Lindstrdm, 1984), muscular pain (Usubiaga et al, 1967;Haldia et al, 1973), adiposa dolorosa (Iwane et al, 1976;Lindstr6m & Lindblom, 1987;Kastrup et al, 'Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Antinociception induced by systemic administration of local anaesthetics depends on a central cholinergic mechanism

Bartolini

Galli

Ghelardini

et al. 1987

British J Pharmacology

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The antinociceptive effects of systemically‐administered procaine, lignocaine and bupivacaine were examined in mice and rats by using the hot‐plate, writhing and tail flick tests. In both species all three local anaesthetics produced significant antinociception which was prevented by atropine (5 mg kg−1, i.p.) and by hemicholinium‐3 (1 μg per mouse, i.c.v.), but not by naloxone (3 mg kg−1, i.p.), α‐methyl‐p‐tyrosine (100 mg kg−1, s.c.), reserpine (2 mg kg−1, i.p.) or atropine methylbromide (5.5 mg kg−1, i.p.). Atropine (5 mg kg−1, i.p.) which totally antagonized oxotremorine (40 μg kg−1, s.c.) antinociception did not modify morphine (5 mg kg−1, s.c.) or baclofen (4 mg kg−1, s.c.) antinociception. On the other hand, hemicholinium, which antagonized local anaesthetic antinociception, did not prevent oxotremorine, morphine or baclofen antinociception. Intracerebroventricular injection in mice of procaine (200 μg), lignocaine (150 μg) and bupivacaine (25 μg), doses which were largely ineffective by parenteral routes, induced an antinociception whose intensity equalled that obtainable subcutaneously. Moreover, the i.c.v. injection of antinociceptive doses did not impair performance on the rota‐rod test. Concentrations below 10−10 m of procaine, lignocaine and bupivacaine did not evoke any response on the isolated longitudinal muscle strip of guinea‐pig ileum, or modify acetylcholine (ACh)‐induced contractions. On the other hand, they always increased electrically‐evoked twitches. The same concentrations of local anaesthetics which induced antinociception did not inhibit acetylcholinesterase (AChE) in vitro. On the basis of the above findings and the existing literature, a facilitation of cholinergic transmission by the local anaesthetics is postulated; this could be due to blockade of presynaptic muscarinic receptors.

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Intravenous lignocaine anÆsthesia

Cited by 69 publications

References 2 publications

Lidocaine Blocks the Hyperpolarization-activated Mixed Cation Current, I h, in Rat Thalamocortical Neurons

Lidocaine Blocks the Hyperpolarization-activated Mixed Cation Current, I h, in Rat Thalamocortical Neurons

Intravenous lidocaine as adjuvant to general anesthesia in renal surgery

Antinociception induced by systemic administration of local anaesthetics depends on a central cholinergic mechanism

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