title: Pretreatment with xenon protected immature rabbit heart from ischaemia/reperfusion injury by opening of the mitoKATP channel.
abstract: BACKGROUND
  The noble gas anaesthetic, xenon has previously been shown to protect the adult myocardium from ischaemia/reperfusion (I/R) injury, however its effect on immature myocardium is unclear. The aim of this study was to investigate the effect of xenon on the isolated immature heart.
  
  
  METHODS
  Isolated, immature (2-3weeks old) New Zealand rabbit hearts were perfused with Krebs-Henseleit buffer via Langendorff-mode. After 20min of baseline equilibration, hearts were pretreated with 75% xenon, 75% xenon+100μM diazoxide, or 75% xenon+100μM 5-hydroxydecanoate, and then subjected to 1h of global ischaemia and 3h of reperfusion.
  
  
  RESULTS
  Pretreatment with 75% xenon significantly improved cardiac function (P<0.01 vs. the I/R group, respectively), limited myocardial infarct size (20.83±2.16%, P<0.01 vs. 35.82±2.14% of the I/R group), reduced cardiac enzyme release (CK-MB, 1.00±0.19IU/L, P<0.01 vs. 0.44±0.14IU/L of the I/R group; LDH, 6.15±1.06IU/L P<0.01 vs. 3.49±0.37IU/L of the I/R group) and decreased apoptosis (6.17±0.56%, P<0.01 vs. 11.31±0.93% of the I/R group). In addition, the mitochondrial structure changes caused by I/R injury were largely prevented by 75% xenon pretreatment (1.37±0.16, P<0.01 vs. 2.32±0.13 of the I/R group). The mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channel opener diazoxide did not influence the effect of xenon, but the specific mitoKATP channel blocker 5-hydroxydecanoate completely abolished this effect.
  
  
  CONCLUSIONS
  Our study demonstrated that pretreatment with 75% xenon protected immature heart from I/R injury, and this protection was probably mediated by preservation of myocardial mitochondria and opening of mitoKATP channel.
authors.affiliation: Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Li
authors.forename: Chunwei
authors.initials: C
authors.lastname: Lian
authors.forename: Ronghua
authors.initials: R
authors.lastname: Zhou
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Xujin
authors.initials: X
authors.lastname: Xiang
authors.forename: Bin
authors.initials: B
authors.lastname: Liu
mesh_terms: D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000494:pharmacology; D003652:Decanoic Acids / Q000009:adverse effects / Q000494:pharmacology; D006880:Hydroxy Acids / Q000009:adverse effects / Q000494:pharmacology; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D009124:Muscle Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism*; D011817:Rabbits; D014978:Xenon / Q000494:pharmacology*
chemical_list: D018685:Anesthetics, Inhalation; D000889:Anti-Arrhythmia Agents; D003652:Decanoic Acids; D006880:Hydroxy Acids; D009124:Muscle Proteins; D015221:Potassium Channels; C117780:mitochondrial K(ATP) channel; D014978:Xenon; C052853:5-hydroxydecanoic acid