Local Anesthetic-Induced Convulsions in Man

Usubiaga, Jose E.; Wikinski, Jaime A.; Ferrero, R.; Usubiaga, Lilia E.; Wikinski, Regina

doi:10.1213/00000539-196609000-00019

Cited by 38 publications

(21 citation statements)

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“…Yoshida et al (1991) recently demonstrated openings of the 235 pS K' channel immediately after the spontaneous action potential in the hippocampal cell, prepared in the same way as in the present study. It might be speculated that seizure following an overdose of a local anaesthetic is related to a possible blocking action of the drug on K+ channels in the central nervous system (Usubiaga et al, 1966;de Jong et al, 1969;Warnick et al, 1971). The present study demonstrates that ionized forms of the local anaesthetics block the Ca2"-activated K+ channels from the cytoplasmic side, in essentially the same manner as for Na+ channels.…”

Section: Introductionsupporting

confidence: 54%

Blockade by local anaesthetics of the single Ca²⁺‐activated K⁺ channel in rat hippocampal neurones

Oda

Yoshida

Ikemoto

1992

British J Pharmacology

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Effects of local anaesthetics on single Ca2+‐activated K+ channels were investigated using the inside‐out configuration of the patch‐clamp technique in single pyramidal neurones, which were freshly dissociated from rat hippocampus by use of proteolytic enzymes. No significant effect was observed when 2 mm benzocaine was applied on either side of the membrane patch, or when 3 mm lignocaine or QX‐314 was applied to the external surface of the membrane. Lignocaine 1 mm, applied to the internal surface, slightly reduced the amplitude of the single K+ channel current. When applied to the internal surface, QX‐314 reduced the amplitude of the K+ channel current, accompanied by an increase in noise in the open channel current, suggesting a fast flickering block. The blocking effect of QX‐314 on the outward current increased with depolarization, suggesting a binding site for the drug at an electrical distance of about 0.5 across the membrane field. The open time histogram showed one exponential component and the closed time histogram showed at least two components. The mean open time of the outward current was increased when the amplitude was reduced by the drugs. The ionized form of the local anaesthetics had a similar action on the Ca2+‐activated K+ channels to that on Na+ channels, that is, they enter into the channel from the cytoplasmic side to induce open channel block. The blocking kinetics, however, might be so fast that they were beyond the frequency response of our recording apparatus, thus the recorded current amplitude was decreased. In contrast the K+ channel was not accessible via hydrophobic pathways for the neutral form, which is also known to block the sodium channel.

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Section: Introductionsupporting

confidence: 54%

Blockade by local anaesthetics of the single Ca²⁺‐activated K⁺ channel in rat hippocampal neurones

Oda

Yoshida

Ikemoto

1992

British J Pharmacology

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“…Clinical symptoms of CNS toxicity showed a similar time onset following both drugs, although the infusion was tolerated significantly less time following lidocaine relative to procaine. These findings were similar to those of Usubiaga et al (1966), which compared even higher doses of lidocaine (1.5 to 3.0 mg/kg/min) and procaine (3.0 to 9.0 mg/kg/min) and used only seizures as their clinical endpoint. The increased therapeutic index of procaine over lidocaine may be a result of procaine’s more rapid clearance through hydroxylation or its effect on sodium channels.…”

Section: Discussionsupporting

confidence: 84%

“…To our knowledge, only Foldes et al (1960) and Usubiaga et al (1966) also directly compared these two medications. Foldes et al (1960) utilized dramatically higher doses than those given in the present study, administering lidocaine (0.5 mg/kg/min) and procaine (1.0 mg/kg/min) for up to 25 minutes or until severe CNS symptoms became evident (i.e.…”

Section: Discussionmentioning

confidence: 99%

Neural response to lidocaine in healthy subjects

Adinoff¹,

Devous²,

Cooper³

et al. 2009

Psychiatry Research: Neuroimaging

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Recent studies suggest that some of cocaine’s central nervous system (CNS) effects may be mediated through its sodium channel inhibiting local anesthetic properties. Local anesthetics that lack cocaine’s strong affinity for the dopamine transporter (DAT) also produce sensory and mood effects, further suggesting a role for this neural pathway. Due to an absence of affinity at the DAT, the local anesthetic lidocaine may offer the potential to assess sodium channel activity in vivo in humans. To assess the utility of lidocaine as a CNS probe, we determined regional cerebral blood flow (rCBF) with single photon emission computed tomography (SPECT) following the intravenous administration of lidocaine (0.5 mg/kg) and compared this response to procaine (0.5 mg/kg and 1.0 mg/kg), a local anesthetic with partial affinity for the DAT, and saline. Infusions were administered in nine healthy female controls over a ten-day period with at least two days between each scan. Increased rCBF was observed following lidocaine, relative to saline, in the insula, caudate, thalamus, thalamus, and posterior cingulate. Decreased rCBF was detected in a different region of the posterior cingulate. In general, increases in rCBF were more marked following lidocaine relative to procaine. Mood and sensory changes following lidocaine were limited and significantly less than those induced by either dose of procaine. There were no significant changes in blood pressure or heart rate following either medication. These findings suggest that lidocaine can be safely used to assess sodium channel function in persons with addictive and other psychiatric disorders.

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“…Our results show that lidocaine is appropriate to perform fetocide: Effective and rapid cessation of the heart activity was obtained with an amount of drug that remained below the toxic doses for the mother 30,31 . This proved sufficient in all cases but one.…”

Section: Discussionmentioning

confidence: 66%

“…The initial dose was based on a lethal dose to be given to a 1000 g 28,29 fetus which can be estimated to be around 100 mg/kg while this would remain within the safe dose regimen for the mother in the event of accidental injection in the maternal circulation (2.8 -4.2 mg/kg) 30 . Failure was empirically defined as being unable to induce permanent asystole with a maximum of 300 mg of lidocaine while remaining below a toxic/convulsant dose for the mother (7 mg/kg) 31 . Therefore, the dose injected was between 7 and 30 mL, depending on the gestational age and was given until cessation of the heart activity.…”

Section: Methodsmentioning

confidence: 99%

The use of lidocaine for fetocide in late termination of pregnancy

Senat¹

2003

BJOG: An International Journal of Obstetrics and Gynaecology

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Local Anesthetic-Induced Convulsions in Man

Cited by 38 publications

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Blockade by local anaesthetics of the single Ca²⁺‐activated K⁺ channel in rat hippocampal neurones

Blockade by local anaesthetics of the single Ca²⁺‐activated K⁺ channel in rat hippocampal neurones

Neural response to lidocaine in healthy subjects

The use of lidocaine for fetocide in late termination of pregnancy

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Local Anesthetic-Induced Convulsions in Man

Cited by 38 publications

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Blockade by local anaesthetics of the single Ca2+‐activated K+ channel in rat hippocampal neurones

Blockade by local anaesthetics of the single Ca2+‐activated K+ channel in rat hippocampal neurones

Neural response to lidocaine in healthy subjects

The use of lidocaine for fetocide in late termination of pregnancy

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Blockade by local anaesthetics of the single Ca²⁺‐activated K⁺ channel in rat hippocampal neurones

Blockade by local anaesthetics of the single Ca²⁺‐activated K⁺ channel in rat hippocampal neurones