The effect of some foreign anions on suxamethonium blockade of the isolated rat diaphragm preparation

Harris, John B.; Leach, G. D. H.

doi:10.1111/j.1476-5381.1970.tb10593.x

Cited by 4 publications

(2 citation statements)

References 37 publications

(50 reference statements)

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“…. , -I ., \ \ OL Our results with prolonged application of decamethonium in vivo in the cat and in the rat (Creese & Maclagan, 1970) are comparable to those obtained by many authors in isolated muscle from the frog (Gissen & Nastuk, 1966), cat (Maclagan, 1962), rat (Thesleff, 1955;Gibberd, 1966;Harris & Leach, 1970), guinea-pig (Jenden, 1955), rabbit (Jenden, Kamijo & Taylor, 1954) and man (Creese, Dillon, Marshall, Sabawalla, Schneider, Taylor & Zinn, 1957). In vitro, as in vivo, the recovery of the twitch during prolonged application of the drug is critically dependent on the dose (Jenden et al, 1954;Gissen & Nastuk, 1966).…”

Section: Discussionsupporting

confidence: 89%

Labelled Decamethonium in Cat Muscle

Creese

Maclagan

1976

British J Pharmacology

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I Tritium-labelled decamethonium was infused intravenously in 12 cats at final rates of 1.3-4.2 nmol kg-' min-' to produce a steady plasma concentration which ranged between 0.21-1.3 gimol/l in different experiments. Muscle contractions were elicited by nerve stimulation and the potential at the end-plate regions of superficial fibres was recorded by extracellular electrodes. 2 Under these conditions, it was not possible to obtain a steady degree of neuromuscular block. The initial decrease in muscle contractions was followed by recovery towards the original value although the concentration of decamethonium in the plasma remained constant, or in some cases rose. The initial depolarization of the end-plate region also waned during the constant infusion of the drug. 3 Once the twitch tension had returned to control values during infusion of the drug, prolongation of the infusion for a total of four hours did not produce a secondary neuromuscular block. 4 Scintillation counting showed that during infusion oflabelled decamethonium the radioactivity ofthe muscles increased progressively with time. The uptake was less in the soleus muscle than in the fastcontracting flexor longus digitorum and extensor longus digitorum muscles. Muscles which had been denervated 12-13 days previously showed a greater uptake of labelled drug than control muscles from the contralateral limb. 5The labelled drug was localized by autoradiography of frozen sections of leg muscles following intra-arterial injection of decamethonium. Grain counts in individual fibres showed that small amounts of decamethonium had entered the muscle fibres along their entire length, and there was increased uptake of the drug into the cell in the region of the end-plate. 6 The mechanisms underlying the waning of the pharmacological response during constant application of depolarizing drugs are discussed.

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Section: Discussionsupporting

confidence: 89%

Labelled Decamethonium in Cat Muscle

Creese

Maclagan

1976

British J Pharmacology

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“…The prejunctional effects of muscle relaxants stressed by many authors (EDWARDS & IKDEA 1962, HUBBARD & SCHMIDT 1963, STANDAERT & ADAMS 1965, FREEMAN 1968, RIKER & OKAMOTO 1969, HARRIS & LEACH 1970, GALINDO 1971 could also be influenced by acid-base changes and therefore explain the decrease in sensitivity for depolarising and the increase in sensitivity for non-depolarising relaxants. Further single fibre studies are needed to differentiate between these possible causes.…”

Section: Discussionmentioning

confidence: 99%

Acidosis and Neuromuscular Blockade

Crul-Sluijter

Crul

1974

Acta Anaesthesiol Scand

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The effect of different types of acidosis on sensitivity to neuromuscular blocking agents was studied in vivo on the tibialis muscle of cats and in vitro in the phrenic nerve diaphragm preparation of the rat. In vivo metabolic acidification was caused by diffusion of weak organic acids, which penetrate easily into the cell and imitate closely the state of metabolic acidosis in man. Respiratory acidosis was caused by inhalation of 10% carbon dioxide in oxygen. In the in vitro experiments, acidification was caused by titration with the same acids as well as hydrochloric acid. pH was lowered to levels just above 7.0. Blank in vivo studies showed that the metabolic acidosis by itself causes no significant depression of indirect muscle contraction, while respiratory acidosis causes only a slight depression. A minor depression was seen in the blank in vitro metabolic acidosis studies.Both succinylcholine and decamethonium blocks are strongly antagonised in vivo and in vitro by metabolic and respiratory acidosis. Pancuronium bromide block was potentiated by metabolic and respiratory acidosis both in the in vivo and in vitro experiments. It is most likely that changes in transmembrane potential are the cause for the changes in sensitivity seen in these experiments. R. B. (1956) Plasma, extracellular and muscle electrolyte responses to acute metabolic acidosis. Calculation of intracellular pH from the distribution of 5,5-dimethyl-2,4-oxazolidinedione (DMO) Application to skeletal muscle of the dog. TOBIN,

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Actions of tetraphenylboron on neuromuscular transmission in the biventer cervicis muscle of the chick

Marshall¹

1970

European Journal of Pharmacology

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The effect of some foreign anions on suxamethonium blockade of the isolated rat diaphragm preparation

Cited by 4 publications

References 37 publications

Labelled Decamethonium in Cat Muscle

Labelled Decamethonium in Cat Muscle

Acidosis and Neuromuscular Blockade

Actions of tetraphenylboron on neuromuscular transmission in the biventer cervicis muscle of the chick

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