title: Effects of myocardial ischemia on the release of cardiac troponin I in isolated rat hearts.
abstract: BACKGROUND
  The twofold aim of this experimental study was (1) to verify the correlation between the duration of ischemia and concentration of cardiac troponin I and (2) to compare the release of cardiac troponin I with histologic findings.
  
  
  METHODS
  Experiments were done on 18 rat hearts, which were perfused according to the Langendorff method, immediately after excision in group I (control group) and after immersion for 3 hours (group II) and 6 hours (group III) in St. Thomas' Hospital solution at 4 degrees C. During reperfusion, the release of cardiac troponin I, creatine kinase isoenzyme MB, and lactate dehydrogenase, the recovery of left ventricular pressure, and heart rates were compared among the three groups. After the experiment, three samples of myocardium (left ventricle, right ventricle, and septum) were taken for histologic examination.
  
  
  RESULTS
  Cardiac troponin I concentration was significantly higher in group III than in groups I and II and in group II compared with group I. Cardiac troponin I concentration increased as the ischemic period increased. The relation between cardiac troponin I release and ischemic duration tended to be linear. Creatine kinase MB and lactate dehydrogenase concentrations did not differ from one group to the other. Left ventricular pressure was not significantly different among the groups. In the control group, no heart had more than 10% of the myocytes affected. One of six hearts in group II and three of six in group III had more than 10% of myocytes affected.
  
  
  CONCLUSIONS
  This experimental study showed (1) that cardiac troponin I is an early marker of ischemic injury and (2) that cardiac troponin I concentration increases as the ischemic period increases. Early cardiac troponin I release appears to correlate with the extent of ischemic injury in rats undergoing buffer perfusion.
authors: Department of Thoracic and Cardiovascular Surgery, Saint-Jacques Hospital, Besançon, France.
authors: S
authors: S
authors: Chocron
authors: K
authors: K
authors: Alwan
authors: G
authors: G
authors: Toubin
authors: B
authors: B
authors: Kantelip
authors: F
authors: F
authors: Clement
authors: J P
authors: JP
authors: Kantelip
authors: J P
authors: JP
authors: Etievent
mesh_terms: D000818:Animals; D001639:Bicarbonates / Q000008:administration & dosage; D015415:Biomarkers / Q000032:analysis; D002122:Calcium Chloride / Q000008:administration & dosage; D002314:Cardioplegic Solutions / Q000008:administration & dosage; D003402:Creatine Kinase / Q000378:metabolism; D006339:Heart Rate; D006346:Heart Septum / Q000378:metabolism / Q000473:pathology; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D016014:Linear Models; D008274:Magnesium / Q000008:administration & dosage; D008297:Male; D017202:Myocardial Ischemia / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D011189:Potassium Chloride / Q000008:administration & dosage; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000008:administration & dosage; D014336:Troponin / Q000378:metabolism*; D019210:Troponin I; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D001639:Bicarbonates; D015415:Biomarkers; D002314:Cardioplegic Solutions; D007527:Isoenzymes; C041711:St. Thomas' Hospital cardioplegic solution; D014336:Troponin; D019210:Troponin I; D012965:Sodium Chloride; D011189:Potassium Chloride; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D008274:Magnesium; D002122:Calcium Chloride