title: Infusion of the beta-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats.
abstract: OBJECTIVE
  Since beta-blocker therapy is known to be effective in patients with an injured heart, such as infarction, we designed the present study to examine the protective effects of infusion of the beta1-selective blocker esmolol on myocardial function in peritonitis-induced septic rats using an isolated working heart preparation.
  
  
  METHODS
  Randomized animal study.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  Thirty-one rats treated with cecal ligation and perforation to evoke peritonitis.
  
  
  METHODS
  After cecal ligation and perforation, rats were randomly allocated to the control group (normal saline 2 mL/hr, n = 11), low-dose esmolol group (10 mg/kg/hr, n = 10), or high-dose esmolol group (20 mg/kg/hr, n = 10). After obtaining blood samples for measurement of arterial lactate and tumor necrosis factor-alpha at 24 hrs, we assessed cardiac output, myocardial oxygen consumption, and cardiac efficiency (cardiac output x peak systolic pressure/myocardial oxygen consumption) at various preloads in an isolated perfused heart preparation.
  
  
  RESULTS
  Esmolol infusion did not cause an elevation of arterial lactate levels but reduced tumor necrosis factor-alpha concentrations vs. the control group (p < .05). Both cardiac output and cardiac efficiency in the esmolol-treated rats were significantly higher throughout the study periods vs. the control group (p < .05).
  
  
  CONCLUSIONS
  Esmolol infusion in sepsis improved oxygen utilization of myocardium and preserved myocardial function.
authors.affiliation: Department of Anesthesiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morisaki
authors.forename: Ryohei
authors.initials: R
authors.lastname: Serita
authors.forename: Michiko
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Kotake
authors.forename: Akitoshi
authors.initials: A
authors.lastname: Ishizaka
authors.forename: Junzo
authors.initials: J
authors.lastname: Takeda
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists; D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology / Q000517:prevention & control*; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D006439:Hemodynamics; D007262:Infusions, Intravenous; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010101:Oxygen Consumption; D011412:Propanolamines / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D002316:Cardiotonic Agents; D016207:Cytokines; D011412:Propanolamines; C036604:esmolol