title: The efficacy and mechanism of dexmedetomidine in myocardial apoptosis via the renin-angiotensin-aldosterone system.
abstract: BACKGROUND
  Pharmacological preconditioning limits myocardial infarct size after ischemia/reperfusion. Dexmedetomidine is an α2-adrenergic receptor agonist used in anesthesia that may have cardioprotective properties against ischemia/reperfusion injury. We investigated whether dexmedetomidine induces cardioprotection against myocardial apoptosis injury.
  
  
  METHODS
  In order to assess the role of dexmedetomidine on myocardial apoptosis, we established a grave scalding rat model. Blood and myocardial tissue from the ventriculus sinister were harvested, then troponin, myocardial apoptosis, and expression of caspase-12, GRP78, and CHOP were assessed.
  
  
  RESULTS
  Dexmedetomidine significantly reduced myocardial apoptosis, improved functional recovery, and reversed myocardial injury induced by grave scalding. The heart rate in the five groups studied was significantly different (p < 0.05). The number of buffy-stained nucleoli in the myocardial cell was highest in the simple scald group. The expression of caspase-12 obviously increased in the simple scald group. The expression of GRP78 and CHOP increased in the simple scald and scald and 50 μg/kg dexmedetomidine groups (p < 0.05).
  
  
  CONCLUSIONS
  The results show that dexmedetomidine (DEX) produces cardioprotection against myocardial apoptosis injury. DEX is not only a useful sedative, but also plays a pivotal role in anesthetic cardioprotection. The potential benefits of DEX protection in high risk cardiovascular patients undergoing surgery are enormous.
authors.affiliation: Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, China Affiliated Union Hospital, Fujian Medical University, China.
authors.forename: Huishu
authors.initials: H
authors.lastname: Wang
authors.affiliation: Affiliated Union Hospital, Fujian Medical University, China.
authors.forename: Siduo
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, China xushiyuan355@163.com.
authors.forename: Shiyuan
authors.initials: S
authors.lastname: Xu
authors.affiliation: Affiliated Union Hospital, Fujian Medical University, China.
authors.forename: Liangcheng
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D053454:Caspase 12 / Q000378:metabolism; D020927:Dexmedetomidine / Q000494:pharmacology*; D000091342:Endoplasmic Reticulum Chaperone BiP; D006339:Heart Rate / Q000187:drug effects; D006360:Heat-Shock Proteins / Q000378:metabolism; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D009206:Myocardium / Q000166:cytology* / Q000648:ultrastructure; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000187:drug effects*; D051742:Transcription Factor CHOP / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; D051742:Transcription Factor CHOP; D020927:Dexmedetomidine; D053454:Caspase 12
keywords: CHOP; Dexmedetomidine; GRP78; myocardial apoptosis