Pre‐and post‐junctional effects of tubocurarine and other nicotinic antagonists during repetitive stimulation in the rat.

Gibb, Alasdair J.; Marshall, Ian

doi:10.1113/jphysiol.1984.sp015245

Cited by 112 publications

(81 citation statements)

References 49 publications

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“…Nicotinic antagonists such as tubocurarine (Liley & North, 1953;Hubbard & Wilson, 1973) and pancuronium (Blaber, 1973) cause such a rundown and in the case of tubocurarine, this rundown has since been shown to be mediated prejunctionally (Magleby et al, 1981;Gibb & Marshall, 1984). In contrast, erabutoxin b does not produce rundown (Gibb & Marshall, 1984) and trimetaphan, produces rundown by a use-dependent block of the receptor activated ion channel (Gibb & Marshall, 1984). Of the drugs used in this study, tubocurarine, pancuronium and hexamethonium have all been shown to be capable ofblocking the receptor-activated ion channel at the frog neuromuscular junction, although in the cases of tubocurarine and pancuronium, only at concentrations around 10 times higher than were used in this study (Lambert et al, 1983 for review).…”

Section: Discussionmentioning

confidence: 99%

Nicotinic antagonists produce differing amounts of tetanic fade in the isolated diaphragm of the rat

Gibb

Marshall

1986

British J Pharmacology

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1 The effects of nicotine antagonists on single twitches, trains of four twitches and tetanic contractions of the isolated diaphragm of the rat were examined. 2 Different drugs were found to produce different amounts of tetanic fade relative to depression of twitch tension. 3 The order of activity from most able, to least able to produce fade was: hexamethonium>trimeta-phan = atracurium = tubocurarine > pancuronium > erabutoxin b. 4 The effect of erabutoxin b was distinctive for its almost complete lack of tetanic fade. 5 3, 4-Diaminopyridine increased tetanic fade produced by tubocurarine, atracurium and hexamethonium, but not that produced by erabutoxin b. 6 It is concluded that nicotinic antagonists act at more than one site at the neuromuscular junction. Assuming block of the postjunctional acetylcholine receptor produces tension depression, a second or third site must be involved in producing tetanic fade. 7 The possibility that tetanic fade results from block of the ion channel associated with the postjunctional acetycholine receptor or from the block of a prejunctional nicotinic receptor is discussed.

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Section: Discussionmentioning

confidence: 99%

Nicotinic antagonists produce differing amounts of tetanic fade in the isolated diaphragm of the rat

Gibb

Marshall

1986

British J Pharmacology

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“…Others have suggested that the binding site involved in the production of fade could be a presynaptic AChR [2][3][4][5][6][7][8]. In evaluation of our data it is important to underscore the fact that all efforts to detect interaction or binding of o~-toxins to putative presynaptic ACh receptors of any type have been unsuccessful [11].…”

Section: Discussionmentioning

confidence: 99%

“…Reports that or-toxins do not cause fade as does curare [5,6,9,10] and do not bind to the presynaptic nerve terminal [11] have been cited as support for this theory [2,5,9]. It has been reported that unlike curare, the or-toxin from Laticauda semifasciata does not cause a fade in end-plate currents [5], nor does it bring about tetanic fade in the isolated rat diaphragm [6]. Similarly, it has been reported that a,-bungarotoxin from Bungarus multicinctus does not cause tetanic fade in the tibialis anterior muscle of the anaesthetized cat [9,10].…”

Section: Introductionmentioning

confidence: 99%

“…It has been proposed that fade is caused in part by a presynaptic effect of curare [2][3][4][5][6][7][8]. Reports that or-toxins do not cause fade as does curare [5,6,9,10] and do not bind to the presynaptic nerve terminal [11] have been cited as support for this theory [2,5,9]. It has been reported that unlike curare, the or-toxin from Laticauda semifasciata does not cause a fade in end-plate currents [5], nor does it bring about tetanic fade in the isolated rat diaphragm [6].…”

Section: Introductionmentioning

confidence: 99%

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Multiple effects of α‐toxins on the nicotinic acetylcholine receptor

Bradley¹,

Pagala²,

Edge³

1987

FEBS Letters

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Very low concentrations (5 nM) of ~-toxin from the venom of Naja naja atra produced a characteristic fade in muscle compound action potential and tetanus induced by repetitive nerve stimulation which was identical to the effects of curare. High concentrations of s-toxin and all concentrations of ~-bungarotoxin reduced the response but produced very little fade in comparison to curare. These results suggest that :t-toxins have more than one effect at the neuromuscular junction.

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“…10 A block by non-depolarizing NBAs would lead to a progressive decrease in the amount of ACh released per stimulus during TOF stimulation, accounting for the TOF fade phenomenon. 8,17,18 Based on this mechanism, differences among drugs in the production of the TOF fade can be accounted for by different affinities for prejunctional receptors, i.e. , the greater the affinity, the greater the TOF fade.…”

Section: A B Cmentioning

confidence: 99%

Train-of-four fade and neuromuscular block in rats: a comparison between pancuronium, vecuronium, and rocuronium

Itoh

Sato

Nitta

et al. 2000

Can J Anesth/J Can Anesth

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Purpose: To clarify the relationship between neuromuscular block and train-of-four fade and to investigate the causes of these drug-dependent differences, we compared the neuromuscular block and TOF fade after pancuronium, vecuronium and rocuronium.Methods: In 24 anesthetized rats, the sciatic nerve was stimulated, and the twitch of left tibialis anterior muscle was recorded. After T 1 (first twitch response) was kept constant at 95% block by administration of pancuronium, vecuronium, or rocuronium (n=8, in each), the TOF fade was measured when T 1 block was decreased to 40% and 20%. In addition, using 24 phrenic nerve-diaphragm preparations, the fade was measured when the T 1 block increased to 20% and 40% by titrating of either one of the three drugs (n=8, in each). Results: In in vivo experiments, the fade produced by pancuronium was greater than that by vecuronium or rocuronium when T 1 block was at 40% (81 ± 9 vs 63 ± 15 and 63 ± 6%, respectively) and at 20% (66 ± 13 vs 34 ± 17 and 40 ± 6%, respectively). In contrast, in in vitro experiments, the differences did not reach significant levels among the three drugs either at 20% (32 ± 19 vs 33 ± 10 and 32 ± 17%) or 40% of block (62 ± 29 vs 65 ± 14 and 55 ± 14%). Conclusions: For vecuronium and rocuronium, the results were similar in vivo and in vitro. For pancuronium, fade was greater in vivo. These results suggest that different neuromuscular blocking agent have different relationships between the fade and the block. In vitro results might not be the same as in vivo, possibly due to pharmacokinetic differences.

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Pre‐and post‐junctional effects of tubocurarine and other nicotinic antagonists during repetitive stimulation in the rat.

Abstract: 6. We conclude that tubocurarine and erabutoxin b reduce the e.p.c. amplitude

Cited by 112 publications

References 49 publications

Nicotinic antagonists produce differing amounts of tetanic fade in the isolated diaphragm of the rat

Nicotinic antagonists produce differing amounts of tetanic fade in the isolated diaphragm of the rat

Multiple effects of α‐toxins on the nicotinic acetylcholine receptor

Train-of-four fade and neuromuscular block in rats: a comparison between pancuronium, vecuronium, and rocuronium

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