title: Dexmedetomidine decreases perioperative myocardial lactate release in dogs.
abstract: The sympatholytic effect of the alpha(2)-adrenergic agonist dexmedetomidine may decrease emergence-related myocardial ischemic load in patients. However, a direct measure of myocardial ischemia, such as myocardial lactate release, is difficult to obtain in patients. Therefore, we studied mongrel dogs and measured myocardial lactate release, myocardial oxygen supply, hemodynamic variables, and neurohumoral indices of the stress response. After the induction of a standardized degree of borderline myocardial ischemia, either dexmedetomidine (dexmed group, n = 9) or normal saline (control group, n = 9) was infused. Measurements were repeated at the end of the anesthetic period and every 10 min during the 90-min emergence period. In the dexmed group, the cumulative emergence-related lactate release was 46% less than in the control group (95% confidence interval, 20%-80%; P = 0.02). Simultaneously, dexmedetomidine increased the endo-/epicardial blood flow ratio by 35% (control group, 0.4 +/- 0.1; dexmed group, 0.6 +/- 0.1; P = 0.03). These antiischemic effects of dexmedetomidine were accompanied by reduced plasma concentrations of norepinephrine (126 versus 577 pg/mL) and epinephrine (158 versus 1909 pg/mL) and a slower heart rate (123 +/- 6 versus 160 +/- 10 bpm, dexmed versus control). The antiischemic effect of dexmedetomidine started before emergence, as evidenced by a decreased prevalence of myocardial lactate release at that time (zero of eight dogs in the dexmed group and four of seven dogs in the control group had lactate release before emergence; P = 0.03).
  
  
  CONCLUSIONS
  Dexmedetomidine decreases plasma catecholamines and heart rate during emergence from anesthesia. In dogs with a coronary stenosis, these sympatholytic effects decrease myocardial lactate release and, therefore, minimize emergence-related myocardial ischemia.
authors.affiliation: *Department of Anesthesiology, University Hospital Maastricht; and †Department of Physiology, Maastricht University, Maastricht, The Netherlands.
authors.forename: Henriëtte M
authors.initials: HM
authors.lastname: Willigers
authors.forename: Frits W
authors.initials: FW
authors.lastname: Prinzen
authors.forename: Paul M
authors.initials: PM
authors.lastname: Roekaerts
authors.forename: Simon
authors.initials: S
authors.lastname: de Lange
authors.forename: Marcel E
authors.initials: ME
authors.lastname: Durieux
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D002395:Catecholamines / Q000097:blood; D003326:Coronary Circulation / Q000187:drug effects; D023921:Coronary Stenosis / Q000473:pathology / Q000601:surgery; D003864:Depression, Chemical; D020927:Dexmedetomidine / Q000494:pharmacology*; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D019344:Lactic Acid / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D013312:Stress, Physiological / Q000503:physiopathology
chemical_list: D000316:Adrenergic alpha-Agonists; D002395:Catecholamines; D019344:Lactic Acid; D020927:Dexmedetomidine