title: Deterioration of myocardial injury due to dexmedetomidine administration after myocardial ischaemia.
abstract: OBJECTIVE
  Dexmedetomidine is a highly selective α-2 adrenergic agonist used perioperatively. Dexmedetomidine's cardioprotective effect after myocardial ischaemia remains unknown. In this study, we administered dexmedetomidine after ischaemia to investigate its ability to protect the cardiac muscle from ischaemia-reperfusion injury in isolated rat hearts.
  
  
  METHODS
  After a 30-min stop of perfusion, isolated rat hearts underwent reperfusion for 120 min. At the initiation of reperfusion, dexmedetomidine was administered for 25 min at concentrations of 0 nM (control group), 1 nM (Dex 1 group), and 10 nM (Dex 10 group). Yohimbine (an α-2 adrenergic antagonist) was administered in the manner as above in another group of isolated rat hearts at a concentration of 1 μM without dexmedetomidine (Yoh group) and at 1 μM with 10 nM dexmedetomidine (Yoh+Dex 10 group). The area of infarction was measured using 2,3,5-triphenyltetrazolium staining.
  
  
  RESULTS
  Dexmedetomidine administration did not influence haemodynamics or the coronary flow (CF), but did increase the myocardial infarct size. Neither concentration of dexmedetomidine affected the infarct size as the Dex 1 and Dex 10 groups had almost the same infarct size. The infarct size was 40.5±2.9% in the control group, 60.9±5.3% in the Dex 1 group, and 60.9±2.8% in the Dex 10 group. The infarct size was reduced in the yohimbine groups. The infarct size was 39.2±3.3% in the Yoh+Dex 10 group and 45.0±3.2% in the Yoh group.
  
  
  CONCLUSIONS
  Dexmedetomidine administration does not influence haemodynamics or CF, but does increase the cardiac infarct size. α-2 Adrenergic stimulation may induce this mechanism.
authors.affiliation: Department of Anaesthesiology and Intensive Care, Hamamatsu University School of Medicine, 1-20-1, Handayama, Higashiku, Hamamatsu, Shizuoka 431-3192, Japan. mimsou@hotmail.com
authors.forename: Soichiro
authors.initials: S
authors.lastname: Mimuro
authors.forename: Takasumi
authors.initials: T
authors.lastname: Katoh
authors.forename: Akira
authors.initials: A
authors.lastname: Suzuki
authors.forename: Shuchun
authors.initials: S
authors.lastname: Yu
authors.forename: Yushi U
authors.initials: YU
authors.lastname: Adachi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Uraoka
authors.forename: Hideki
authors.initials: H
authors.lastname: Sano
authors.forename: Shigehito
authors.initials: S
authors.lastname: Sato
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists / Q000008:administration & dosage / Q000009:adverse effects*; D058669:Adrenergic alpha-2 Receptor Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D020927:Dexmedetomidine / Q000008:administration & dosage / Q000009:adverse effects*; D006439:Hemodynamics / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015016:Yohimbine / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D015016:Yohimbine; D020927:Dexmedetomidine