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Eicosapentaenoic acid preserves diaphragm force generation following endotoxin administration.doc

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Eicosapentaenoic acid preserves diaphragm force generation following endotoxin administration

Supinskietal.CriticalCare2010,14:R35 /content/14/2/R35 RESEARCH OpenAccess Eicosapentaenoicacidpreservesdiaphragmforce generationfollowingendotoxinadministration GeraldSSupinski*,JonasVanags,LeighAnnCallahan Abstract Introduction:Infectionsproducesevererespiratorymuscleweakness,whichcontributestothedevelopmentof respiratoryfailure.Aneffective,safetherapytopreventrespiratorymuscledysfunctionininfectedpatientshasnot beendefined.Thisstudyexaminedtheeffectofeicosapentaenoicacid(EPA),animmunomodulatorthatcanbe safelyadministeredtopatients,ondiaphragmforcegenerationfollowingendotoxinadministration. Methods:Ratswereadministeredthefollowing(n=5/group):(a)saline,(b)endotoxin,12mg/kgIP,(c)endotoxin+ EPA(1.0g/kg/d),and(d)EPAalone.Diaphragmswereremovedandmeasurementsmadeofthediaphragmforce- frequencycurve,calpainactivation,caspaseactivation,andproteincarbonyllevels. Results:Endotoxinelicitedlargereductionsindiaphragmspecificforcegeneration(P0.001),andincreased diaphragmcaspaseactivation(P0.01),calpainactivation(P0.001)andproteincarbonyllevels(P0.01).EPA administrationattenuatedendotoxin-inducedreductionsindiaphragmspecificforce,withmaximumspecificforce levelsof27±1,14±1,23±1,and24±1N/cm2,respectively,forcontrol,endotoxin,endotoxin+EPA,andEPA treatedgroups(P0.001).EPAdidnotpreventendotoxininducedcaspaseactivationorproteincarbonyl formationbutsignificantlyreducedcalpainactivation(P0.02). Conclusions:Thesedataindicatethatendotoxin-inducedreductionsindiaphragmspecificforcegenerationcan bepartiallypreventedbyadministrationofEPA,anontoxicbiopharmaceuticalthatcanbesafelygiventopatients. Wespeculatethatitmaybepossibletoreduceinfection-inducedskeletalmuscleweaknessincriticallyillpatients byadministrationofEPA. Introduction muscle calpain proteolytic system [5-7]. Each of these Infections producesevere respiratory muscleweakness, pathways, moreover, istheoretically capable ofinterac- whichcontributestothedevelopmentofrespiratoryfail- ting with skeletal muscle contractile protein