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dc.contributor.authorOchala, Julien
dc.contributor.authorAhlbeck, Karsten
dc.contributor.authorRadell, Peter J.
dc.contributor.authorEriksson, Lars I.
dc.contributor.authorLarsson, Lars
dc.contributor.editorMei, Lin
dc.date.accessioned2012-10-26T16:27:00Z
dc.date.available2012-10-26T16:27:00Z
dc.date.issued2011-06-14en_US
dc.identifier.citationPLoS One. 2011 Jun 14; 6(6):e20876en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid21695079en_US
dc.identifier.doi10.1371/journal.pone.0020876en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/657
dc.description.abstractThe basic mechanisms underlying acquired generalized muscle weakness and paralysis in critically ill patients remain poorly understood and may be related to prolonged mechanical ventilation/immobilization (MV) or to other triggering factors such as sepsis, systemic corticosteroid (CS) treatment and administration of neuromuscular blocking agents (NMBA). The present study aims at exploring the relative importance of these factors by using a unique porcine model. Piglets were all exposed to MV together with different combinations of endotoxin-induced sepsis, CS and NMBA for five days. Peroneal motor nerve conduction velocity and amplitude of the compound muscle action potential (CMAP) as well as biceps femoris muscle biopsy specimens were obtained immediately after anesthesia on the first day and at the end of the 5-day experimental period. Results showed that peroneal nerve motor conduction velocity is unaffected whereas the size of the CMAP decreases independently of the type of intervention, in all groups after 5 days. Otherwise, despite a preserved size, muscle fibre specific force (maximum force normalized to cross-sectional area) decreased dramatically for animals exposed to MV in combination with CS or/and sepsis. These results suggest that the rapid declines in CMAP amplitude and in force generation capacity are triggered by independent mechanisms with significant clinical and therapeutic implications.
dc.rightsOchala et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectAnatomy and Physiologyen_US
dc.subjectMusculoskeletal Systemen_US
dc.subjectMusculoskeletal Anatomyen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectNeuroscienceen_US
dc.subjectNeurophysiologyen_US
dc.subjectNeuromuscular Junctionen_US
dc.subjectMedicineen_US
dc.subjectAnatomy and Physiologyen_US
dc.subjectMusculoskeletal Systemen_US
dc.subjectMuscleen_US
dc.subjectMuscle Functionsen_US
dc.subjectMusculoskeletal Anatomyen_US
dc.subjectCell Physiologyen_US
dc.subjectCritical Care and Emergency Medicineen_US
dc.subjectSepsisen_US
dc.subjectVentilatory Supporten_US
dc.subjectNeurologyen_US
dc.subjectMovement Disordersen_US
dc.subjectNeuromuscular Diseasesen_US
dc.titleFactors Underlying the Early Limb Muscle Weakness in Acute Quadriplegic Myopathy Using an Experimental ICU Porcine Modelen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3114861en_US
dc.contributor.corporatenameDepartment of Neurology
refterms.dateFOA2019-04-10T00:28:31Z
html.description.abstractThe basic mechanisms underlying acquired generalized muscle weakness and paralysis in critically ill patients remain poorly understood and may be related to prolonged mechanical ventilation/immobilization (MV) or to other triggering factors such as sepsis, systemic corticosteroid (CS) treatment and administration of neuromuscular blocking agents (NMBA). The present study aims at exploring the relative importance of these factors by using a unique porcine model. Piglets were all exposed to MV together with different combinations of endotoxin-induced sepsis, CS and NMBA for five days. Peroneal motor nerve conduction velocity and amplitude of the compound muscle action potential (CMAP) as well as biceps femoris muscle biopsy specimens were obtained immediately after anesthesia on the first day and at the end of the 5-day experimental period. Results showed that peroneal nerve motor conduction velocity is unaffected whereas the size of the CMAP decreases independently of the type of intervention, in all groups after 5 days. Otherwise, despite a preserved size, muscle fibre specific force (maximum force normalized to cross-sectional area) decreased dramatically for animals exposed to MV in combination with CS or/and sepsis. These results suggest that the rapid declines in CMAP amplitude and in force generation capacity are triggered by independent mechanisms with significant clinical and therapeutic implications.


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