Bupivacaine Toxicity in Pregnant and Nonpregnant Ewes

Morishima, Hisayo O.; Pedersen, H.; Finster, M.; Hiraoka, Haruhiko; Tsuji, Akira; Feldman, Hal S.; Arthur, G. R.; Covino, Benjamín G.

doi:10.1097/00132582-198603000-00020

Cited by 8 publications

(11 citation statements)

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“…The convulsive doses and plasma concentrations of bupivacaine at the onset of convulsions were comparable to those noted in a previous report. 21 The brain/plasma concentration ratio of bupivacaine in the B group at the onset of convulsions was also comparable to that reported by Morishima et al 22 Despite the lower plasma concentration of bupivacaine in the QB group than in the B group at the onset of convulsions, the cumulative doses of bupivacaine required to induce convulsions were comparable in these two groups. Although the reason for this discordance in our findings is not clear, ephedrine may have increased cardiac output, resulting in the increased hepatic blood flow and systemic clearance of bupivacaine.…”

Section: Measurement Of Lidocaine Megx and Bupivacaine In Plasma Andsupporting

confidence: 84%

The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats

Funao

Oda

Tanaka

et al. 2003

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : To examine whether inhibition of P-glycoprotein (P-gp) activity by quinidine affects the central nervous system toxicity of lidocaine and racemic bupivacaine (bupivacaine).M Me et th ho od ds s: : Forty male Sprague-Dawley rats were randomly divided into four groups (n = 10). Fifteen minutes following administration of 15 mg·kg ) was infused until convulsions occurred. Concentrations of lidocaine and its primary metabolite, monoethylglycinexylidide (MEGX) and bupivacaine in plasma and in the brain at the onset of convulsions were measured by high-performance liquid chromatography.R Re es su ul lt ts s: : There were no differences in the dose of lidocaine required to induce convulsions between the L and QL groups. There were no differences in the concentrations of total (L = 17.2 ± 3.5, QL = 16.6 ± 2.6 µg·mL ) in plasma, total lidocaine or MEGX in the brain at the onset of convulsions between the L and QL groups. The dose of bupivacaine required to induce convulsions was comparable in the B and QB groups. At the onset of convulsions, plasma concentrations of both total (B = 4.9 ± 1.1, QB = 4.0 ± 0.6 µg·mL -1 , P = 0.03) and unbound bupivacaine (B = 1.4 ± 0.6, QB = 0.9 ± 0.2 µg·mL -1 , P = 0.02) were significantly lower in the QB group than in the B group. There were no differences in concentration of total bupivacaine in the brain between the B and QB groups.C Co on nc cl lu us si io on n: : These results suggest that quinidine inhibited P-gp activity, resulting in increased brain/plasma concentration ratio of bupivacaine, but not of lidocaine, and decreased the threshold of plasma concentration for bupivacaine-induced convulsions. (L = 17,2 ± 3,5, QL = 16,6 ± 2, ) et libre (L = 7,8 ± 2,5, QL = 7,3 ± 2, ), entre le MEGX total (L = 1,2 ± 0,5, QL = 1,3 ± 0, ) et libre (L = 0,9 ± 0,5, QL = 0,8± 0,4 (B = 4,9 ± 1,1, QB = 4,0 ± 0, , P = 0,03) et libre (B = 1,4 ± 0,6, QB = 0,9 ± 0 The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats La quinidine, un inhibiteur de P-glycoprotéine, abaisse le seuil des convulsions induites par la bupivacaïne, mais non par la lidocaïne, chez les rats Objectif : Vérifier si l'inhibition de l'activité des P-glycoprotéines (P-gp

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Section: Measurement Of Lidocaine Megx and Bupivacaine In Plasma Andsupporting

confidence: 84%

The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats

Funao

Oda

Tanaka

et al. 2003

Can J Anesth/J Can Anesth

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“…The level causing cardiovascular collapse to CNS toxicity ratio (CC/CNS) has been estimated in animal studies. 16 Local anaesthetics with higher potency and lipophilicity such as bupivacaine have a lower CC/CNS ratio as compared with that of lidocaine (3 vs. 7). Therefore, bupivacaine toxicity can occur with few premonitory symptoms of CNS excitation.…”

Section: Discussionmentioning

confidence: 99%

A Lady with Confusion and Seizure after Ingestion of Lidocaine for Dyspepsia

Li¹,

Lee

Lau

2009

Hong Kong Journal of Emergency Medicine

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Lau Fei Lung, FRCP(Edin), FHKCEM, FHKAM(Emergency Medicine)We report a 29-year-old lady who developed confusion, agitation and seizure after the ingestion of a selfmixture of 3 grams of lidocaine with antacid for treatment of dyspepsia. She developed two episodes of seizure requiring diazepam, propofol and intubation .There was no significant cardiac toxicity and she was discharged on day 3. This is the first reported adult case of seizure in the literature after intentional ingestion of lidocaine for treatment of dyspepsia. The use of local anaesthetic in gastrointestinal cocktail for dyspepsia and its safety are highlighted. Advances in the management of local anaesthetic overdose are also discussed. (Hong Kong j.emerg.med. 2009;16:41-45) 29 3

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“…Feldman et al [7] noted an incidence of lethal ventricular fibrillation in awake dogs receiving a convulsant dose of bupivacaine. Significant incidences of cardiac arrest or cardiac arrhythmias with bupiva caine were noted in cyclopropane-anesthe tized rats [8] and in adult sheep [9]. Lynch [10] also reported that bupivacaine depressed myocardial contraction in the guinea pig.…”

Section: Introductionmentioning

confidence: 99%

Effects of Bupivacaine on Contraction and Membrane Potential in Isolated Canine Papillary Muscles

Shibuya

Momose²,

Ito³

1993

Pharmacology

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The effects of bupivacaine on myocardial contraction and membrane potential were examined in isolated canine right ventricular papillary muscles. Bupivacaine (10^–6 to 10^–4 mol/l) produced a dose-dependent and reversible decrease in the electrically induced contractile response of canine right ventricular papillary muscles. The inhibitory effects of bupivacaine on contraction were more pronounced at high stimulation frequencies (2 and 3 Hz) than at low frequency (<1 Hz). The resting membrane potential was not affected by bupivacaine. The maximal upstroke velocity of the action potential was reduced by 10^–6 mol/l bupivacaine (74 ± 28% of control), and these effects were also dose dependent. At 10^–4 mol/l, bupivacaine blocked fast action potentials in normal Tyrode’s solution. Furthermore, bupivacaine (10^–4 and 10^-3 mol/l) decreased both slow action potential duration and associated contractions in high-K⁺ (26 mmol/l) Tyrode’s solution in the presence of isoproterenol. Our results suggest that low concentrations of bupivacaine depress contraction mainly due to an Na⁺ channel block, whereas at higher concentration, this local anesthetic may block Ca²⁺ channels.

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Bupivacaine Toxicity in Pregnant and Nonpregnant Ewes

Cited by 8 publications

References 0 publications

The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats

The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats

A Lady with Confusion and Seizure after Ingestion of Lidocaine for Dyspepsia

Effects of Bupivacaine on Contraction and Membrane Potential in Isolated Canine Papillary Muscles

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