Intensive Care Medicine

, Volume 37, Issue 8, pp 1344–1351 | Cite as

Effects of esmolol on systemic and pulmonary hemodynamics and on oxygenation in pigs with hypodynamic endotoxin shock

  • Jerome Aboab
  • Veronique Sebille
  • Mercé Jourdain
  • Jacques Mangalaboyi
  • Miloud Gharbi
  • Arnaud Mansart
  • Djillali AnnaneEmail author



The aim of this experimental study is to investigate cardiovascular tolerance of blockade of beta-adrenergic receptors in an endotoxin model.


Prospective, randomized, controlled study.


Animal laboratory in a university medical center.


Ten anesthetized, mechanically ventilated pigs were challenged with intravenous lipopolysaccharide (LPS) to achieve a status of profound hypodynamic shock. Systemic and pulmonary hemodynamics and cardiac output were continuously monitored throughout the 5-h study period, and blood samples were taken at baseline (T − 30 min), 1 h from the beginning of LPS infusion (T + 60 min), and every 2 h (T + 180 min and T + 300 min). Animals were randomly assigned to continuous intravenous esmolol infusion titrated to decrease heart rate by 20% or isotonic saline.


Esmolol decreased heart rate by 20%, while in the saline group, heart rate increased by 7% and 22% at T + 180 min and T + 300 min, respectively (p < 0.001). In esmolol-treated animals, cardiac index decreased by 9% at T + 180 min and by 2% at T + 300 min, and in controls by 14% at T + 180 min and by 27% at T + 300 min (p = 0.870). In esmolol-treated animals, median (interquartile range, IQR) stroke index was 31 (6) and 47 (11) ml/min/m2 at T + 180 min and T + 300 min, respectively, and decreased steadily from 45 (20) to 18 (13) ml/min/m2 in controls (p = 0.030). There were no significant differences between groups for any other hemodynamics variables, except for systemic vascular resistance (SVR) (p = 0.017).


In large animals with endotoxemic shock, continuous infusion of esmolol, a selective beta-1 adrenergic blocker, titrated to decrease heart rate by 20%, was well tolerated and may offset LPS-induced cardiac dysfunction by a preload positive effect.


Septic shock Beta blockade Esmolol Hemodynamics Animal model 



This study was funded by a grant from the Société de Réanimation de Langue Française.

Supplementary material

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Supplementary material 5 (DOC 26 kb)


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Copyright information

© Copyright jointly held by Springer and ESICM 2011

Authors and Affiliations

  • Jerome Aboab
    • 1
    • 4
  • Veronique Sebille
    • 2
  • Mercé Jourdain
    • 3
  • Jacques Mangalaboyi
    • 3
  • Miloud Gharbi
    • 1
  • Arnaud Mansart
    • 4
  • Djillali Annane
    • 1
    • 4
    Email author
  1. 1.Service de Réanimation, Hôpital Raymond Poincaré, AP-HPUniversité de Versailles Saint QuentinGarchesFrance
  2. 2.Laboratoire de Biomathématiques-Biostatistique, EA 4275, Faculté de PharmacieUniversité de NantesNantes Cedex 1France
  3. 3.Service de RéanimationHôpital Roger SalengroLilleFrance
  4. 4.Laboratoire d’étude de la réponse neuroendocrine au sepsis- EA 4342Université de Versailles Saint QuentinGarchesFrance

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