title: Progression of myocardial necrosis during reperfusion of ischemic myocardium.
abstract: BACKGROUND
  The occurrence of myocyte necrosis during reperfusion of ischemic myocardium is controversial. This study measured myocardial 2-deoxyglucose uptake, correlated with histology, to determine whether loss of viability occurred during reperfusion of ischemic myocardium.
  
  
  RESULTS
  In 12 anesthetized dogs, the left anterior descending coronary artery was occluded for 90 minutes before 4 hours reperfusion. Myocardial blood flow was measured by microspheres and the tracers 14C-2-deoxyglucose and 18F-2-deoxyglucose were injected intravenously after 5 and 180 minutes of reperfusion, respectively. After 240 minutes, the heart was stained with thioflavin-S (size of no-reflow zone) and triphenyl-tetrazolium chloride (TTC, extent of necrosis). Samples from normal, salvaged, and necrotic myocardium were counted for 14C- and 18F-deoxyglucose and microspheres. With the use of a three-compartment model of 2-deoxyglucose uptake, the rate constant k3 for phosphorylation of 14C- and 18F-2-deoxyglucose was calculated for each sample. Viability was defined as k3> or = 0.125 min(-1) (predictive accuracy 88% versus electron microscopy and 97% versus TTC). Among 58 samples from no-reflow regions, 97% were nonviable after 5 minutes of reperfusion (k3=0.096 +/- 0.027 min[-1]). Among 164 samples from salvaged myocardium, 95% were viable after both 5 and 180 minutes of reperfusion (k3=0.170 +/- 0.056 min[-1] P<.01 versus no-reflow). Among 179 samples from infarcted myocardium, mean k3 after 5 minutes of reperfusion was 0.184 +/- 0.070 min(-1) and 65% of samples were viable, but after 180 minutes of reperfusion mean k3 had decreased to 0.077 +/- 0.032 min(-1) (P<.0001) and 98% of samples were nonviable.
  
  
  CONCLUSIONS
  A large proportion of samples from infarcted myocardium are viable at the end of the ischemic period but lose viability during the first hours of reperfusion.
authors.affiliation: Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Md 21205, USA.
authors.forename: K
authors.initials: K
authors.lastname: Matsumura
authors.forename: R W
authors.initials: RW
authors.lastname: Jeremy
authors.forename: J
authors.initials: J
authors.lastname: Schaper
authors.forename: L C
authors.initials: LC
authors.lastname: Becker
mesh_terms: D000818:Animals; D003847:Deoxyglucose / Q000493:pharmacokinetics; D018450:Disease Progression; D004285:Dogs; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000150:complications* / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000009:adverse effects; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000737:chemistry / Q000473:pathology / Q000648:ultrastructure
chemical_list: D003847:Deoxyglucose