title: Different effects of postconditioning on myocardial no-reflow in the normal and hypercholesterolemic mini-swines.
abstract: BACKGROUND
  Postconditioning with multiple very short coronary occlusions immediately after prolonged ischemia has been found to reduce infarction size. However, it remains unknown whether postconditioning under the normal or hypercholesterolemic condition can also reduce myocardial no-reflow for which endothelial dysfunction is an important mechanism.
  
  
  METHODS
  Twenty-four normal mini-swines were randomized into 3 study groups: 8 in control, 8 in postconditioning, 8 in sham-operated group. Twenty-four hypercholesterolemic mini-swines were also randomized into 3 study groups: 8 in control, 8 in postconditioning, 8 in sham-operated group. Acute myocardial infarction and reperfusion model was created with 3 h occlusion of the left anterior descending coronary artery followed by two-hour reperfusion. Coronary ligation area (LA) and area of no-reflow were determined with pathological means (Path).
  
  
  RESULTS
  Compared with the normal control group, postconditioning under the normal condition significantly improved endothelial function, decreased area of no-reflow (Path: from 81.3+/-3.9% to 54.3+/-3.69% of LA, P<0.01) and reduced necrosis area from 98.5+/-2.35% to 76.1+/-5.6% of LA (P<0.05-0.01). However, compared with the normal control group, postconditioning under the hypercholesterolemic condition did not significantly modify endothelial function, area of no-reflow and necrosis area (P>0.05).
  
  
  CONCLUSIONS
  These findings support the concept that postconditioning under the normal condition can reduce the area of no-reflow and necrosis area, while postconditioning under the hypercholesterolemic condition cannot. The beneficial effect of postconditioning on myocardial no-reflow could be due to its protection of endothelial function.
authors.affiliation: Department of Cardiology, Cardiovascular Institute and Fu-Wai Heart Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Bei Li Shi Road 167, West City District, 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: Chuan-Jue
authors.initials: CJ
authors.lastname: Cui
authors.forename: Run-Lin
authors.initials: RL
authors.lastname: Gao
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D004730:Endothelium, Vascular / Q000503:physiopathology; D006937:Hypercholesterolemia / Q000503:physiopathology* / Q000628:therapy; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control* / Q000628:therapy; D015425:Myocardial Reperfusion; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D013552:Swine; D013556:Swine, Miniature
chemical_list: D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III