title: [Effect of adenosine on endothelin-1 in the infarcted reflow and no-reflow myocardium of mini-swine].
abstract: OBJECTIVE
  To evaluate the effect of adenosine on endothelin-1 (ET-1) after acute myocardial infarction (AMI) and reperfusion and explore the possible mechanism of no-reflow.
  
  
  METHODS
  Twenty-four mini-swine were randomized into three study groups: control group (n=8), adenosine treated group (n=8), and sham-operated group (n=8). The mini-swine in the groups were subjected to 3 hours of coronary occlusion, followed by 60 minutes of reperfusion except those in the sham-operated group. The levels of ET-1 in blood sample, normal, infracted reflow and no-reflow myocardium were evaluated by radioimmuno-assay (RIA). The gene expressions of ET-1 in normal, infracted reflow and no-reflow myocardium were quantified by reverse transcription-polymerase chain reaction.
  
  
  RESULTS
  In both control group and adenosine group, compared with that at the baseline, ET-1 in blood sample significantly increased at 5 minutes and 180 minutes of left anterior descending coronary artery occlusion, as well as 5 and 60 minutes of reperfusion (all P < 0.01). In adenosine group, the levels of ET-1 were significantly lower than those in the control group (P < 0.05, P < 0.01). In both control group and adenosine group, compared with that in normal myocardium, ET-1 levels in both infarcted reflow and no-reflow myocardium significantly increased (both P < 0.01), with the level of ET-1 in no-reflow myocardium significantly higher than that in infarcted reflow myocardium (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01). In both control and adenosine groups, compared with that in normal myocardium, the gene expression of ET-1 in infarcted reflow myocardium was significantly up-regulated (P < 0.01), while that of ET-1 in. no-reflow myocardium significantly down-regulated (P < 0.01). In adenosine group, the level of ET-1 in infarcted reflow myocardium was significantly lower than that in the control group (P < 0.01).
  
  
  CONCLUSIONS
  The endothelium injury may be one of the important mechanisms for no-reflow phenomenon. Adenosine cay prevent endothelium from injury to reduce no-reflow.
authors.affiliation: Department of Coronary Heart Disease, Cardiovascular Institute and Fuwai Hospital, CAMS and PUMC, Beijing 100037, China.
authors.forename: Jing-lin
authors.initials: JL
authors.lastname: Zhao
authors.forename: Yue-jin
authors.initials: YJ
authors.lastname: Yang
authors.forename: Shi-jie
authors.initials: SJ
authors.lastname: You
authors.forename: Zhi-cheng
authors.initials: ZC
authors.lastname: Jing
authors.forename: Yong-jian
authors.initials: YJ
authors.lastname: Wu
authors.forename: Wei-xian
authors.initials: WX
authors.lastname: Yang
authors.forename: Ji-lin
authors.initials: JL
authors.lastname: Chen
authors.forename: Run-lin
authors.initials: RL
authors.lastname: Gao
authors.forename: Zai-jia
authors.initials: ZJ
authors.lastname: Chen
mesh_terms: D000241:Adenosine / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D013552:Swine; D013556:Swine, Miniature
chemical_list: D019332:Endothelin-1; D000241:Adenosine