The effects of esmolol and dexmedetomidine on myocardial oxygen consumption during sympathetic stimulation in dogs.
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.


METHODS
Experimental study.


METHODS
Laboratory of university.


METHODS
Eleven anesthetized dogs.


METHODS
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.


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.
Willigers
Henriëtte M
HM
Department of Anesthesiology, University Hospital, Maastricht, Maastricht, the Netherlands.
Prinzen
Frits W
FW
Roekaerts
Paul M H J
PM
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D020927:Dexmedetomidine / Q000494:pharmacology*; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects*; D011412:Propanolamines / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D020927:Dexmedetomidine; C036604:esmolol; D009638:Norepinephrine