Resistance to d-Tubocurarine in Lower Motor Neuron Injury Is Related to Increased Acetylcholine Receptors at the Neuromuscular Junction

Hogue, Charles W.; Itani, Mohamad I.; Martyn, J. A. J.

doi:10.1097/00000542-199010000-00016

Cited by 58 publications

(24 citation statements)

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“…Also, expression of γ-AChR after denervation has clinical significance, because the two subtypes have different electrophysiological and drug-binding properties [10] . Previous data have confirmed that denervated skeletal muscle displays resistance to NDMRs [5,11] and that potencies of different NDMRs are different at ε-AChR and γ-AChR [12][13][14] . Interestingly, Narimatsu et al [15] observed that the magnitude of sepsis-induced attenuation of potencies of NDMRs depends on the kind of neuromuscular blocker.…”

Section: Introductionmentioning

confidence: 84%

“…Denervation in turn causes pharmacological changes in skeletal muscle, with the main changes leading to potentially lethal hyperkalemia in response to the depolarizing muscle relaxant succinylcholine and resistance to nondepolarizing muscle relaxants (NDMRs), typified by d-tubocurarine (dTC) [2,3] . Up-regulation (increase) of nicotinic acetylcholine receptors (nAChR) explains some of these pharmacological responses [4,5] . nAChRs include two subtypes: the adult form (ε-AChR) composed of α 2 βδε subunits and the fetal form (γ-AChR) containing α 2 βδγ subunits [6,7] .…”

Section: Introductionmentioning

confidence: 99%

“…Clinically-used NDMRs competitively occupy the α δ and α ε (or α γ ) sites of the nAChR to achieve muscle relaxation during surgery and artificial ventilation. Denervation causes up-regulation of nAChRs and AChRγ mRNA [5,9] to increase the doses of NDMRs needed to competitively bind to nAChR. Also, expression of γ-AChR after denervation has clinical significance, because the two subtypes have different electrophysiological and drug-binding properties [10] .…”

Section: Introductionmentioning

confidence: 99%

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Different magnitude of resistance to nondepolarizing muscle relaxants in the denervated mouse skeletal muscle

Wang

Yang

et al. 2010

Acta Pharmacol Sin

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Aim: To test the hypothesis that different magnitude of resistance of denervated skeletal muscle to nondepolarizing muscle relaxants (NDMRs) is related to their varying potencies at ε-AChR and γ-AChR. Methods: Both innervated and denervated mouse muscle cells, and human embryonic kidney 293 (HEK293) cells expressing ε-AChR or γ-AChR were used. The effects of NDMRs on nAChR were explored using whole-cell patch clamp technique. Results: NDMRs vecuronium (VEC), atracurium (ATR) and rocuronium (ROC) produced reversible, dose-dependent inhibition on the currents induced by 30 μmol/L acetylcholine both in innervated and denervated skeletal muscle cells. Compared to those obtained in innervated skeletal muscle cells, denervation shifted the concentration-response curves rightward and significantly increased the 50% inhibitory concentration (IC 50 ) values (VEC: from 11.2 to 39

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Section: Introductionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Different magnitude of resistance to nondepolarizing muscle relaxants in the denervated mouse skeletal muscle

Wang

Yang

et al. 2010

Acta Pharmacol Sin

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“…This association has been established with conditions which include burns, denervation, and the chronic administration of a muscle relaxant or an anticonvulsant drug. [13][14][15] AChR up-regulation has not been described with HPT; however, muscular disease in HPT appears to be neurogenic. 16 This neurogenic muscular atrophy may result in up-regulation of AChRs and subsequent hyposensitivity to NDMRs.…”

Section: éLéments Cliniquesmentioning

confidence: 98%

Reduced duration of muscle relaxation with rocuronium in a normocalcemic hyperparathyroid patient

Munir

Jaffar

Arshad

et al. 2003

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : To report a case of reduced duration of action of rocuronium in a patient with normocalcemic hyperparathyroidism (HPT).C Cl li in ni ic ca al l f fe ea at tu ur re es s: : A 56-yr-old patient with primary HPT, who had had surgical resection of three and a half parathyroid glands nine months previously, was referred to our institution for further investigation of a persistent increase in parathyroid hormone. Preoperatively, the patient had a normal serum ionized and total calcium. The patient was diagnosed with a persistent parathyroid adenoma and was scheduled for an elective parathyroidectomy.

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“…However, thermal injury and other forms of critical illness cause denervation changes in skeletal muscle, which results in decreased potencies of nondepolarizing muscle relaxants (NDMRs) [1,2]. Skeletal muscle denervation causes up-regulation of nicotinic acetylcholine receptors (nAChRs) and expression de novo of the fetal-type nicotinic acetylcholine receptor (γ-AChR) [3][4][5].…”

Section: Brief Communication (Original)mentioning

confidence: 99%

Effects of skeletal muscle denervation on potency of rocuronium

et al. 2011

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Background:Rocuronium is an alternative to succinylcholine for rapid tracheal intubation after major thermal injury and other forms of critical illness that cause denervation changes in skeletal muscle. Rocuronium may decrease the potencies of non-depolarizing muscle relaxants. Objectives: Examine whether potency of rocuronium changed during the first month after denervation, and investigate the effects of skeletal muscle denervation on potency of rocuronium. Methods: The denervation mouse model was developed to create denervated individual cells from the flexor digitorum brevis of the hindfoot. The skeletal muscle cells were examined at day 0 in the innervated control and days 1, 4, 7, 14, 21, and 28 in the denervation group. Nicotinic acetylcholine receptors in the cells were activated with 30 M acetylcholine, alone or in combination with various concentrations of rocuronium. Currents were recorded with a whole-cell patch-clamp technique. Results: Rocuronium reversibly inhibited acetylcholine-activated currents in a dose-dependent fashion at different times after denervation. The inhibition concentration for the half-maximal responses of rocuronium increased 1.2-(p >0.05), 1.8-, 2.8-, 2.3-, 2.1-, and 1.9-fold (p <0.01) at day 1, 4, 7, 14, 21, and 28 after denervation, respectively, compared to that at day 0 after denervation. Conclusion: Rocuronium dose required to achieve satisfactory clinical effects changed at different durations after skeletal muscle denervation.

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Resistance to d-Tubocurarine in Lower Motor Neuron Injury Is Related to Increased Acetylcholine Receptors at the Neuromuscular Junction

Cited by 58 publications

References 0 publications

Different magnitude of resistance to nondepolarizing muscle relaxants in the denervated mouse skeletal muscle

Different magnitude of resistance to nondepolarizing muscle relaxants in the denervated mouse skeletal muscle

Reduced duration of muscle relaxation with rocuronium in a normocalcemic hyperparathyroid patient

Effects of skeletal muscle denervation on potency of rocuronium

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