Quantification of myocardial infarct size after coronary reperfusion by serum cardiac myosin light chain II in conscious dogs.
The effects of early coronary artery reperfusion on the relation between the extent of myocardial infarction and serum levels of cardiac myosin light chain II or plasma creatine kinase levels were evaluated in the conscious dog. Hydraulic occluders were placed on the left anterior descending arteries of 38 dogs. Seven to 10 days later, myocardial infarction was produced. Coronary reperfusion was performed 3 hours (group A1, n = 13) and 6 hours (group A2, n = 12) after the occlusion. In the other 13 dogs, coronary occlusion was sustained throughout the course of the experiment (group B). Seven days after the occlusion, the heart was cut from the apex to the base into 4-mm slices, and infarct size was determined macroscopically. Rapid appearance and early peaking of creatine kinase were observed in group A. Cumulative release of creatine kinase significantly correlated with infarct size in group A (infarct size ranged from 0.1 to 20.1 g, r = 0.90) and group B (from 0.6 to 26.8 g, r = 0.91). However, since creatine kinase release in group A was greater in comparison with that from infarcts of the same size in group B, the slope of the regression line for group A was significantly steeper (p less than 0.05). Cardiac myosin light chain II appeared as early as creatine kinase did and continued to be elevated for 7 days. A very close relation was observed between infarct size and total cardiac myosin light chain II release (r = 0.87 for group A, and r = 0.88 for group B) or peak level of light chain II (r = 0.85 for group A, and r = 0.81 for group B). In addition, the slopes of the regression lines for infarct size and both peak and total release of light chain II did not differ between group A and group B. On histological examination, viable myocardium was frequently observed in the epicardium of the ischemic area in group A1; therefore, infarct size was greater in group B than in group A1 (p less than 0.05). Also, myocardial creatine kinase content in the epicardium of the center of the ischemic area in group A1 was greater than that in group B. Cardiac myosin light chain II release in group A1 was less than that in group B, whereas no difference was found in plasma creatine kinase release among groups A1, A2, and B.(ABSTRACT TRUNCATED AT 250 WORDS)
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
M
M
Isobe
R
R
Nagai
K
K
Yamaoki
H
H
Nakaoka
F
F
Takaku
Y
Y
Yazaki
D000818:Animals; D015415:Biomarkers / Q000097:blood*; D003402:Creatine Kinase / Q000032:analysis; D004285:Dogs; D006352:Heart Ventricles / Q000473:pathology; D007527:Isoenzymes; D009203:Myocardial Infarction / Q000473:pathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D015879:Myosin Subfragments; D009218:Myosins / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*
D015415:Biomarkers; D007527:Isoenzymes; D015879:Myosin Subfragments; D010446:Peptide Fragments; D003402:Creatine Kinase; D009218:Myosins