title: A porcine model of acute quadriplegic myopathy: a feasibility study.
abstract: BACKGROUND
  The mechanisms underlying acute quadriplegic myopathy (AQM) are poorly understood, partly as a result of the fact that patients are generally diagnosed at a late stage of the disease. Accordingly, there is a need for relevant experimental animal models aimed at identifying underlying mechanisms.
  
  
  METHODS
  Pigs were mechanically ventilated and exposed to various combinations of agents, i.e. pharmacological neuromuscular blockade, corticosteroids and/or sepsis, for a period of 5 days. Electromyography and myofibrillar protein and mRNA expression were analysed using sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE), confocal microscopy, histochemistry and real-time polymerase chain reaction (PCR).
  
  
  RESULTS
  A decreased compound muscle action potential, normal motor nerve conduction velocities, and intact sensory nerve function were observed. Messenger RNA expression, determined by real-time PCR, of the myofibrillar proteins myosin and actin decreased in spinal and cranial nerve innervated muscles, suggesting that the loss of myosin observed in AQM patients is not solely the result of myofibrillar protein degradation.
  
  
  CONCLUSIONS
  The present porcine AQM model demonstrated findings largely in accordance with results previously reported in patients and offers a feasible approach to future mechanistic studies aimed at identifying underlying mechanisms and developing improved diagnostic tests and intervention strategies.
authors.affiliation: Department of Clinical Neurophysiology, Uppsala University, Sweden.
authors.forename: H
authors.initials: H
authors.lastname: Norman
authors.forename: K
authors.initials: K
authors.lastname: Kandala
authors.forename: R
authors.initials: R
authors.lastname: Kolluri
authors.forename: H
authors.initials: H
authors.lastname: Zackrisson
authors.forename: J
authors.initials: J
authors.lastname: Nordquist
authors.forename: S
authors.initials: S
authors.lastname: Walther
authors.forename: L I
authors.initials: LI
authors.lastname: Eriksson
authors.forename: L
authors.initials: L
authors.lastname: Larsson
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology; D000818:Animals; D001623:Betamethasone / Q000494:pharmacology; D018076:DNA, Complementary / Q000096:biosynthesis / Q000235:genetics; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004591:Electrophoresis, Polyacrylamide Gel; D004594:Electrophysiology; D004731:Endotoxins / Q000633:toxicity; D005240:Feasibility Studies; D005260:Female; D006651:Histocytochemistry; D008406:Masseter Muscle / Q000294:innervation* / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000473:pathology; D009135:Muscular Diseases / Q000209:etiology* / Q000473:pathology; D003473:Neuromuscular Nondepolarizing Agents / Q000494:pharmacology; D010197:Pancuronium / Q000494:pharmacology; D010543:Peroneal Nerve / Q000502:physiology; D011782:Quadriplegia / Q000150:complications* / Q000473:pathology; D012313:RNA / Q000096:biosynthesis / Q000302:isolation & purification; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D012121:Respiration, Artificial; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018805:Sepsis / Q000473:pathology; D013127:Spinal Nerves / Q000502:physiology; D013552:Swine
chemical_list: D000305:Adrenal Cortex Hormones; D018076:DNA, Complementary; D004731:Endotoxins; D003473:Neuromuscular Nondepolarizing Agents; D012333:RNA, Messenger; D012313:RNA; D001623:Betamethasone; D010197:Pancuronium