beta-Blockers in sepsis: reexamining the evidence.
Sepsis remains the leading cause for noncardiac intensive care unit deaths in the United States. Despite recent advances in the treatment of this devastating condition, mortality and morbidity remain unacceptably high. Sepsis is characterized by a multitude of pathophysiological changes that include inflammation, metabolic derangements, hemodynamic alterations, and multiorgan dysfunction. Unfortunately, several studies of treatment modalities aimed at correcting one or more of the underlying derangements have led to disappointing results. New treatment modalities are needed. beta-Receptor blockers have long been used for a variety of conditions such as coronary artery disease, congestive heart failure, and arterial hypertension. Recent data suggest that beta-blocker effects on metabolism, glucose homeostasis, cytokine expression, and myocardial function may be beneficial in the setting of sepsis. Although treating a potentially hypotensive condition with a drug with antihypertensive properties may initially seem counterintuitive, the metabolic and immunomodulatory properties of beta-blockers may be of benefit. It is the purpose of this review to discuss the effects of beta-blockers on the following: (1) metabolism, (2) glucose regulation, (3) the inflammatory response, (4) cardiac function, and (5) mortality in sepsis.
Novotny
Nathan M
NM
Departments of Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Lahm
Tim
T
Markel
Troy A
TA
Crisostomo
Paul R
PR
Wang
Meijing
M
Wang
Yue
Y
Ray
Rinki
R
Tan
Jiangning
J
Al-Azzawi
Dalia
D
Meldrum
Daniel R
DR
D000284:Administration, Oral; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004731:Endotoxins / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D007249:Inflammation; D008070:Lipopolysaccharides / Q000378:metabolism; D008954:Models, Biological; D009206:Myocardium / Q000378:metabolism; D011412:Propanolamines / Q000494:pharmacology; D018805:Sepsis / Q000188:drug therapy*
D000319:Adrenergic beta-Antagonists; D016207:Cytokines; D004731:Endotoxins; D008070:Lipopolysaccharides; D011412:Propanolamines; D005947:Glucose; C036604:esmolol