title: Loss of ectonucleotidases from the coronary vascular bed after ischemia-reperfusion in isolated rat heart.
abstract: BACKGROUND
  Ectonucleotidase plays an important role in the regulation of cardiac function by controlling extracellular levels of adenine nucleotides and adenosine. To determine the influence of ischemia-reperfusion injury on ectonucleotidase activity in coronary vascular bed, we compared the metabolic profile of adenine nucleotides during the coronary circulation in pre- and post-ischemic heart.
  
  
  METHODS
  Langendorff-perfused rat hearts were used to assess the intracoronary metabolism of adenine nucleotides. The effects of ischemia on the adenine nucleotide metabolism were examined after 30 min of ischemia and 30 min of reperfusion. Adenine nucleotide metabolites were measured by high performance liquid chromatography.
  
  
  RESULTS
  ATP, ADP and AMP were rapidly metabolized to adenosine and inosine during the coronary circulation. After ischemia, ectonucleotidase activity of the coronary vascular bed was significantly decreased. In addition, the perfusate from the ischemic heart contained a considerable amount of enzymes degrading ATP, AMP and adenosine. Immunoblot analysis revealed that the perfusate from the ischemic heart dominantly contained ectonucleoside triphosphate diphosphohydrolase 1, and, to a lesser extent, ecto-5'-nucleotidase. The leakage of nucleotide metabolizing enzymes from the coronary vascular bed by ischemia-reperfusion was more remarkable in aged rats, in which post-ischemic cardiac dysfunction was more serious.
  
  
  CONCLUSIONS
  Ectonucleotidases were liberated from the coronary vascular bed by ischemia-reperfusion, resulting in an overall decrease in ectonucleotidase activity in the post-ischemic coronary vascular bed. These results suggest that decreased ectonucleotidase activity by ischemia may exacerbate subsequent reperfusion injury, and that levels of circulating ectonucleotidase may reflect the severity of ischemic vascular injury.
authors.forename: Kaoru
authors.initials: K
authors.lastname: Takahashi-Sato
authors.forename: Masahiro
authors.initials: M
authors.lastname: Murakawa
authors.forename: Junko
authors.initials: J
authors.lastname: Kimura
authors.forename: Masa-aki
authors.initials: MA
authors.lastname: Ito
authors.forename: Isao
authors.initials: I
authors.lastname: Matsuoka
mesh_terms: D015720:5'-Nucleotidase / Q000097:blood; D000227:Adenine Nucleotides / Q000008:administration & dosage / Q000097:blood*; D000241:Adenosine / Q000008:administration & dosage / Q000097:blood; D000251:Adenosine Triphosphatases / Q000097:blood; D000375:Aging / Q000097:blood; D000818:Animals; D015703:Antigens, CD / Q000097:blood; D001081:Apyrase / Q000097:blood; D003331:Coronary Vessels / Q000201:enzymology*; D004730:Endothelium, Vascular / Q000201:enzymology; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009708:Nucleotidases / Q000097:blood; D010727:Phosphoric Diester Hydrolases / Q000097:blood; D011755:Pyrophosphatases / Q000097:blood*; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000201:enzymology* / Q000503:physiopathology
chemical_list: D000227:Adenine Nucleotides; D015703:Antigens, CD; D009708:Nucleotidases; C018775:adenosine monophosphatase; D015720:5'-Nucleotidase; D010727:Phosphoric Diester Hydrolases; C065962:ectonucleotide pyrophosphatase phosphodiesterase 1; D000251:Adenosine Triphosphatases; D011755:Pyrophosphatases; D001081:Apyrase; C067869:CD39 antigen; D000241:Adenosine
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