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Effect of remote ischemic preconditioning on phosphorylated protein signaling in children undergoing tetralogy of fallot repair: A randomized controlled trial
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نویسنده
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pepe s. ,liaw n.y. ,hepponstall m. ,sheeran f.l. ,yong m.s. ,d'udekem y. ,cheung m.m. ,konstantinov i.e.
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منبع
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journal of the american heart association - 2013 - دوره : 2 - شماره : 3
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چکیده
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Background-our previous randomized controlled trial demonstrated cardiorespiratory protection by remote ischemic preconditioning (ripc) in children before cardiac surgery. however,the impact of ripc on myocardial prosurvival intracellular signaling remains unknown in cyanosis. ripc may augment phosphorylated protein signaling in myocardium and circulating leukocytes during tetralogy of fallot (tof) repair. methods and results--children (n=40) undergoing tof repair were double-blind randomized to ripc (n=11 boys,9 girls) or control (sham ripc: n=9 boys,11 girls). blood samples were taken before,immediately after,and 24 hours after cardiopulmonary bypass. resected right ventricular outflow tract muscle and leukocytes were processed for protein expression and mitochondrial respiration. there was no difference in age (7.1±3.4 versus 7.1±3.4 months),weight (7.7±1.8 versus 7.5±1.9 kg),or bypass or aortic cross-clamp times between the groups (control versus ripc,mean±sd). no differences were seen between the groups for an increase in the ratio of phosphorylated to total protein for protein kinase b,p38 mitogen activated protein kinase,signal transducer and activator of transcription 3,glycogen synthase kinase 3b,heat shock protein 27,connexin43,or markers associated with promotion of necrosis (serum cardiac troponin i),apoptosis (bax,bcl-2),and autophagy (parkin,beclin-1,lc3b). a high proportion of total proteins were in phosphorylated form in control and ripc myocardium. in leukocytes,mitochondrial respiration and assessed protein levels did not differ between groups. conclusions--in patients with cyanotic heart disease,a high proportion of proteins are in phosphorylated form. ripc does not further enhance phosphorylated protein signaling in myocardium or circulating leukocytes in children undergoing tof repair. clinical trial registration--url: (http://www.anzctr.org.au/trial_view.aspxid=335613. unique identifier: australian new zealand clinical trials registry number actrn12610000496011. © 2013 the authors.
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کلیدواژه
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Cyanosis; Heart; Mitochondria; Pediatric surgery; Remote ischemic preconditioning; Tetralogy of Fallot
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آدرس
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heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne, Australia, heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne, Australia, department of paediatrics,university of melbourne,melbourne, Australia, heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne, Australia, heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne,australia,cardiac surgery,royal children's hospital,melbourne,vic 3052, Australia, heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne,australia,cardiac surgery,royal children's hospital,melbourne,vic 3052, Australia, heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne,australia,departments of cardiology,royal children's hospital,melbourne,vic 3052, Australia, heart research group,murdoch childrens research institute,university of melbourne,melbourne,australia,department of paediatrics,university of melbourne,melbourne,australia,cardiac surgery,royal children's hospital,melbourne,vic 3052, Australia
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Authors
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