title: Dodecafluoropentane emulsion elicits cardiac protection against myocardial infarction through an ATP-Sensitive K+ channel dependent mechanism.
abstract: OBJECTIVE
  Dodecafluoropentane emulsion (DDFPe) is a perfluorocarbon with high oxygen dissolving, transport, and delivery capacity that may offer the potential to limit ischemic injury prior to clinical reperfusion. Here we investigated the cardiac protective potential of DDFPe in a mouse model of myocardial infarction.
  
  
  METHODS
  Myocardial infarction was initiated by permanent ligation of the left anterior descending (LAD) coronary artery. Mice were administered vehicle or 5-hydroxydecanoate (5-HD) intravenously 10 min before LAD occlusion followed by a single intravenous administration of vehicle or DDFPe immediately after occlusion. Heart tissue and serum samples were collected 24 after LAD occlusion for measurement of infarct size and cardiac troponin I (cTnI) levels, respectively.
  
  
  RESULTS
  DDFPe treatment reduced infarct size by approximately 72% (36.9 ± 4.2% for vehicle vs 10.4 ± 2.3% for DDFPe; p < 0.01; n = 6-8) at 24 h. Serum cTnI levels were similarly reduced by DDFPe (35.0 ± 4.6 ng/ml for vehicle vs 15.8 ± 1.6 ng/ml for DDFPe; p < 0.01; n = 6-8). Pretreatment with 5-HD, a mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) inhibitor, blocked the reduction in infarct size (29.2 ± 4.4% for 5-HD vs 35.4 ± 7.4% for 5-HD+DDFPe; p = 0.48; n = 6-8) and serum cTnI levels (27.4 ± 5.1 ng/ml for 5-HD vs 34.6 ± 5.3 ng/ml for 5-HD+DDFPe; p = 0.86; n = 6-8) by DDFPe.
  
  
  CONCLUSIONS
  Our data indicate a cardiac protective role of DDFPe that persists beyond its retention time in the body and is dependent on mitoK(ATP), an important mediator of ischemic preconditioning induced cardiac protection.
authors.affiliation: Department of Pharmacology; College of Medicine, University of Arizona, 1501 N. Campbell Ave, Tucson, AZ, 85724, USA.
authors.forename: Joshua
authors.initials: J
authors.lastname: Strom
authors.forename: Trevor
authors.initials: T
authors.lastname: Swyers
authors.forename: David
authors.initials: D
authors.lastname: Wilson
authors.forename: Evan
authors.initials: E
authors.lastname: Unger
authors.forename: Qin M
authors.initials: QM
authors.lastname: Chen
authors.forename: Douglas F
authors.initials: DF
authors.lastname: Larson
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism; D003652:Decanoic Acids / Q000494:pharmacology; D005466:Fluorocarbons / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006880:Hydroxy Acids / Q000494:pharmacology; D054086:KATP Channels / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism; D010420:Pentanes
chemical_list: D000255:Adenosine Triphosphate; D003652:Decanoic Acids; D005466:Fluorocarbons; D006880:Hydroxy Acids; D054086:KATP Channels; C052853:5-hydroxydecanoic acid; C008806:perfluoropentane; D010420:Pentanes