Blockade of Adrenergic and Cholinergic Transmissions by Emetine

Ng, K. K. F.

doi:10.1111/j.1476-5381.1966.tb01889.x

Cited by 11 publications

(5 citation statements)

References 20 publications

(11 reference statements)

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“…This conclusion is in direct contrast to that reached by Ng (1966) and Salako (1970). It is difficult to reconcile our differing points of view, particularly when it is considered that both Ng (1966) and Salako (1970) mainly described the acute effects of (-)-emetine administration to isolated or in situ preparations.…”

Section: Discussioncontrasting

confidence: 56%

“…Neither can we deny the possibility that there may be a slight, barely measurable effect of (-)-emetine on the safety factor of neuromuscular transmission in treated animals. However, it seems unlikely that the drug seriously impairs neuromuscular transmission either by inducing a neuropathy (Young & Tudhope, 1926) or by affecting the neuromuscular junction directly (Ng, 1966;Salako, 1970). It would appear, therefore, that (-)-emetine myopathy is a condition caused by the direct effects of the drug on skeletal muscle fibres.…”

Section: Discussionmentioning

confidence: 99%

“…This is rather larger than normal (0.2-0.6 mV: these laboratories, unpublished) and probably reflects the atrophy that was noted in many of these muscles. The relationship between fibre diameter and miniature endplate potential amplitude was demonstrated unequivocally by Katz & Thesleff (1957) to be the It has been suggested (Ng, 1966) that the cause of muscular weakness seen during (-)-emetine therapy is an action of (-)-emetine 'at or near the neuromuscular junction ' and Salako (1970) has suggested that the drug has a 'tubocurarine-like action' on the neuromuscular junction. If an action at either a presynaptic or a post-synaptic site were primarily responsible for muscle weakness, the implication would be that either individual muscle fibres or entire motor-units were paralysed.…”

Section: Physiologymentioning

confidence: 99%

“…The precise cause of the weakness is not known, and it has been variously reported that emetine is capable of blocking transmission at ganglia and neuromuscular junctions (Ng, 1966;Salako, 1970) and that it is capable of directly damaging skeletal muscle fibres 'without recognizable morphological or physiological alteration in the neural components of the motor unit' (Duane & Engel, 1970). However, the role of the peripheral ' Present address: Queen Elizabeth Hospital, Woodville,South Australia,5011. nervous system in the pathogenesis of (-)-emetineinduced muscle weakness is difficult to study because, under certain circumstances, the drug is capable of inhibiting protein synthesis (Groilman, 1966(Groilman, , 1968Johnson, Donahue & Jondorf, 1971).…”

Section: Introductionmentioning

confidence: 99%

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Emetine Myopathy in the Rat

Bradley¹,

Fewings²,

Harris³

et al. 1976

British J Pharmacology

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(–)‐Emetine (0.25‐2.0 mg/kg i.p.) was administered to rats for up to 220 days. At doses of 1.0 mg/kg or less, the animals continued to gain weight but more slowly than the untreated control animals. The physiological changes in the muscles from these animals were minimal; there was a small reduction in both the resting membrane potential and in the maximum rate of rise of the action potential. There was no atrophy or loss of muscle fibres although in the occasional muscle, hyaline fibres, necrotic fibres and split fibres were observed. There was a focal loss of myofibrillar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide tetrazolium reductase (NADH‐TR) in Type II and Type III fibres, but no such loss in Type I fibres. The animals receiving 2.0 mg/kg of (–)‐emetine gained weight slowly for up to 20 days but then rapidly lost weight and by 30 days they were weak and emaciated. The muscles from these animals were severely atrophied and the total muscle wet weight was reduced by almost 20%. The strength of the muscles from these animals was measured in vitro using direct stimulation. They were weaker than normal both in absolute terms and when expressed in terms of tension developed/unit wet weight. There was no evidence of either functional or structural denervation but surgically denervated muscles from animals in this group were indistinguishable from denervated muscles from normal rats. Severe structural damage was obvious in the fibres of both extensor digitorum longus and soleus. Necrotic, hyaline and splitting fibres were common and the focal loss of myofibrillar ATPase and NADH‐TR activity was extensive and occurred in Type I fibres as well as in Type II and Type III fibres. It is concluded that the muscular weakness induced by (–)‐emetine is due to a direct effect on the muscle fibres and that this occurs at a subcellular level. There is no evidence that functional or structural denervation plays any role in the aetiology of emetine myopathy in the rat.

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Physiologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Emetine Myopathy in the Rat

Bradley¹,

Fewings²,

Harris³

et al. 1976

British J Pharmacology

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“…In addition to this, it exhibits interesting anti-inflammatory effects (Valipour, 2022). The activity of Emetine on intestinal contraction reported as early as the mid-20th century, depends on the modulation of both cholinergic and adrenergic receptors (Ng, 1966), an activity in agreement with the modulation of gastrointestinal effects in Long COVID-19.…”

Section: Isoquinoline Alkaloidsmentioning

confidence: 93%

Long COVID‐19 gastrointestinal related disorders and traditional Chinese medicine: A network target‐based approach

Mattioli,

Frosini,

Corazza

et al. 2024

Phytotherapy Research

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The significant number of individuals impacted by the pandemic makes prolonged symptoms after COVID‐19 a matter of considerable concern. These are numerous and affect multiple organ systems. According to the World Health Organization (WHO), prolonged gastrointestinal issues are a crucial part of post‐COVID‐19 syndrome. The resulting disruption of homeostasis underscores the need for a therapeutic approach based on compounds that can simultaneously affect more than one target/node. The present review aimed to check for nutraceuticals possessing multiple molecular mechanisms helpful in relieving Long COVID‐19‐specific gastrointestinal symptoms. Specific plants used in Keywords Chinese Medicine (TCM) expected to be included in the WHO Global Medical Compendium were selected based on the following criteria: (1) they are widely used in the Western world as natural remedies and complementary medicine adjuvants; (2) their import and trade are regulated by specific laws that ensure quality and safety (3) have the potential to be beneficial in alleviating intestinal issues associated with Long COVID‐19. Searches were performed in PubMed, Elsevier, Google Scholar, Scopus, Science Direct, and ResearchGate up to 2023. Cinnamomum cassia, Glycyrrhiza uralensis, Magnolia officinalis, Poria cocos, Salvia miltiorrhiza, Scutellaria baicalensis, and Zingiber officinalis were identified as the most promising for their potential impact on inflammation and oxidative stress. Based on the molecular mechanisms of the phytocomplexes and isolated compounds of the considered plants, their clinical use may lead to benefits in gastrointestinal diseases associated with Long COVID‐19, thanks to a multiorgan and multitarget approach.

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