Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat

Edwards, Jonathan P.; Hatton, Paul; Little, R. A.; Pennington, Richard A.; Wareham, Anthony C.

doi:10.1002/(sici)1097-4598(199912)22:12<1660::aid-mus7>3.0.co;2-j

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…As sepsis (501,502,508,711) and nonseptic critical illness, i.e., thermal injury and burns (180,454,462,463), have been reported to attenuate the action of nondepolarizing blocking agents, such as d-tubocurarine or rocuronium, a series of studies were performed to determine the underlying mechanisms of this rather unexpected facilitation of neuromuscular transmission in animal models of experimental sepsis, with sepsis as the only confounding condition inducing muscle weakness. Direct exposure of frog sartorius muscle to Escherichia coli endotoxin (10 g/ml) resulted in elevations of miniature-endplate potential (MEPP) frequencies without changing MEPP amplitudes.…”

Section: B Neuromuscular Transmission In Sepsis and Systemic Inflammmentioning

confidence: 99%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

294

329

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Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

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Section: B Neuromuscular Transmission In Sepsis and Systemic Inflammmentioning

confidence: 99%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

294

329

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“…The effect of a 20% or greater BSA full-thickness dermal burn injury on animal mass and growth has been described previously in detail. 8,40 Burn injury reduces both food intake and body weight for the first few days after the injury. The 20% BSA burn produced a small, nonsignificant decrease in whole-animal body weight relative to pre-burn body weight at 1 day and 3 days following the burn, but burned animals regained some of their lost weight by 7 days.…”

Section: Effect Of Burn Injury On Bodymentioning

confidence: 99%

Peripheral axon caliber and conduction velocity are decreased after burn injury in mice

et al. 2005

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Peripheral neuropathies are reported to arise as a result of the systemic inflammatory response produced by a full-thickness cutaneous burn injury. This study was designed to characterize the magnitude and time course of functional and morphological changes in peripheral axons that arise after a full-thickness dermal burn injury in an animal model. A 20% body surface area (20% BSA) full-thickness dermal burn was applied to the back of C57BL6 female mice. Longitudinal H- and M-wave recordings were used to determine the conduction velocities (CV) of large myelinated motor and sensory axons in the tibial nerve of sham control and burn-injured mice. Motor CVs were significantly reduced from 6 h to 28 days after the burn, and sensory CVs were significantly reduced from 7 to 14 days after the burn. Morphological evaluation also showed that the mean caliber of large axons in tibial nerves and L5 ventral and dorsal roots in burned mice was significantly decreased. The results demonstrate that both functional and morphological deficits may be produced in peripheral nerve axons at sites well removed from a full-thickness dermal burn injury. The neural deficits may contribute to changes in neuromuscular transmission and the development of limb and respiratory muscle weakness that also accompany burn injury.

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“…According to previous studies, the venom of A. crassicauda increases the release of acetylcholine at the neuromuscular junction by both increasing quantal content and the release after single shock stimulation (Vatanpour, 2003[ 34 ]; Edwards et al, 1999[ 10 ]). Since acetylcholine triggers muscle contraction (Cetin et al, 2020[ 5 ]), the muscle spasms observed in the current study in people poisoned by A. crassicauda in northern Khuzestan may be due to the activity of one or more components of this scorpion's venom responsible for the increase in acetylcholine release.…”

Section: Discussionmentioning

confidence: 99%

Intraspecific differences in Androctunus crassicauda venom and envenomation symptoms

Safdarian

Vazirianzadeh

Ghorbani

et al. 2022

EXCLI Journal; 21:Doc1222; ISSN 1611-2156

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Envenomation by Androctunus crassicauda is very frequent in Iran, especially in the south-west . This scorpion is one of the six scorpions whose venom is used to prepare anti-venom. Using HPLC, we discovered venom components of A. crassicauda varies from one specimen to another depending on geographical location, and this result is confirmed by those first found in various symptoms of A. crassicauda sting in envenomed persons from two separate geographical places (north and south of Khuzestan province). There was a significant relationship between symptoms and location of envenomation by A. crassicauda . Muscle spasm was more dominant in envenomed people from Northern cities, and venom chromatogram analysis showed the presence of at least six main sharp peaks in Northern A. crassicauda rather than Southern A. crassicauda . It shows intraspecific differences in venom of A. crassicauda that must be considered in treatment of stung people from different geographical locations as well as in the preparation of anti-venom. See also Figure 1 (Fig. 1) .

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Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat

Cited by 5 publications

References 27 publications

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Peripheral axon caliber and conduction velocity are decreased after burn injury in mice

Intraspecific differences in Androctunus crassicauda venom and envenomation symptoms

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