Document Detail

The effects of esmolol and dexmedetomidine on myocardial oxygen consumption during sympathetic stimulation in dogs.
MedLine Citation:
PMID:  16750737     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: The purpose of this study was to compare the potential of the beta(1)-adrenergic receptor blocker esmolol and the alpha(2)-adrenergic receptor agonist dexmedetomidine to suppress the cardiovascular and neuroendocrine response to a sympathetic stimulus. DESIGN: Experimental study. SETTING: Laboratory of university. PARTICIPANTS: Eleven anesthetized dogs. INTERVENTIONS: Catheters for arterial and coronary venous blood sampling and calculation of myocardial oxygen consumption were inserted. Pressure sensors were placed in the aorta, left ventricle, and a carotid artery. Flow probes were placed around the aortic root and around the left anterior descending coronary artery. Esmolol was infused (loading dose of 1 mg/kg, infusion of 0.3 mg/kg/h), and the adequacy of beta-blockade was checked. Thirty minutes after stopping esmolol, dexmedetomidine infusion was started (loading dose of 1 microg/kg, infusion of 1.5 microg/kg/min). Occlusion of both carotid arteries was used as a sympathetic stimulus before and during infusion of esmolol and before and during infusion of dexmedetomidine. MEASUREMENTS AND MAIN RESULTS: The variables were measured just before and during sympathetic stimulation, and changes were calculated. Both drugs suppressed the increase in dPdT(max). Dexmedetomidine suppressed the increase in plasma norepinephrine and the increase in systemic vascular resistance (dexmedetomidine 4% +/- 4% and esmolol 25% +/- 19% increase, p = 0.02). Esmolol attenuated the heart rate response (esmolol 2% +/- 2% and dexmedetomidine 20% +/- 18% increase, p = 0.02). However, dexmedetomidine decreased baseline heart rate more than esmolol; therefore, the absolute maximal heart rate during sympathetic stimulation was lower in the presence of dexmedetomidine (dexmedetomidine 119 +/- 14 and esmolol 141 +/- 15 beats/min, p = 0.01). Neither drug suppressed the increase in myocardial oxygen consumption. CONCLUSIONS: Both esmolol and dexmedetomidine have the potential to suppress some of the cardiovascular and neuroendocrine changes to a sympathetic stimulus but neither drug abolished the increase in myocardial oxygen consumption.
Henriëtte M Willigers; Frits W Prinzen; Paul M H J Roekaerts
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-04-05
Journal Detail:
Title:  Journal of cardiothoracic and vascular anesthesia     Volume:  20     ISSN:  1053-0770     ISO Abbreviation:  J. Cardiothorac. Vasc. Anesth.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-05     Completed Date:  2006-10-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9110208     Medline TA:  J Cardiothorac Vasc Anesth     Country:  United States    
Other Details:
Languages:  eng     Pagination:  364-70     Citation Subset:  IM    
Department of Anesthesiology, University Hospital, Maastricht, Maastricht, the Netherlands.
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MeSH Terms
Adrenergic alpha-Agonists / pharmacology*
Adrenergic beta-Antagonists / pharmacology*
Dexmedetomidine / pharmacology*
Heart Rate / drug effects
Myocardium / metabolism*
Norepinephrine / blood
Oxygen Consumption / drug effects*
Propanolamines / pharmacology*
Sympathetic Nervous System / physiology*
Vascular Resistance / drug effects
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Adrenergic beta-Antagonists; 0/Propanolamines; 113775-47-6/Dexmedetomidine; 51-41-2/Norepinephrine; 84057-94-3/esmolol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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