作者: Celeste C. Finnerty , David N. Herndon
DOI: 10.1016/J.YASU.2013.02.001
关键词:
摘要: Severe burn injuries result in metabolic and physiological derangements that persist throughout the acute rehabilitative stages.1-3 This hypermetabolic response is driven by supraphysiologic elevations stress hormones, catecholamines, inflammatory mediators.2, 3 Increased peripheral lipolysis,4 increased muscle wasting,5 elevated resting energy expenditure,6 suppressed immune function7 characterize post response. Although initial catecholamine-induced protective supportive of survival,8 prolonged can be detrimental either impedes recovery or leads to organ failure death.5 In addition increasing skeletal catabolism, catecholamine levels also cause lipolysis, expenditure, cardiac severely burned patients.9 The actions catecholamines on cardiovascular system are largely mediated alpha- (α-) beta- (β-) adrenergic receptors. To mitigate effects chronically following injury, blockade β-1 β-2 adrenoreceptors has been achieved with non-selective β1,2-adrenoreceptor antagonist propranolol.9-17 Despite notion blocking would negatively impact hemodynamic responsiveness,9, 10 studies have demonstrated signaling improves pediatric patient outcomes. 9-19 Reductions work accompanied decreased hepatic steatosis, concurrent increases protein anabolism. Few adverse events associated propranolol use.13-15 Propranolol administration massively patients may a standard care for pharmacological amelioration not-so-distant future.