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Articles |
1
Department of Medicine, University of Kobe, Kobe, Japan.
2
Departments of Pathology and Cardiology, Washington
University, St. Louis, MO.
3
Department of Medicine, Section of Cardiology, Baylor
College of Medicine, 6550 Fannin, MS SM677, Houston, TX 77030.
a Author for correspondence. Fax 713-790-4348; e-mail dweaver{at}bmc.tmc.edu
Creatine kinase (CK) isoenzymes MM, MB, and BB are located primarily in
the cell cytosol, and increased CKMB in plasma is the hallmark of
myocardial infarction. However, whether CK is released with reversible
ischemic injury remains controversial. Here, we assessed plasma CK
activity—cytosolic and mitochondrial CK—in serial samples (every 10
min for 60 min, then hourly or every 4 h for 48 h) from 46
conscious dogs after transient or sustained coronary occlusion. Four
dogs were sham-operated (controls); four underwent sustained coronary
occlusion (96 h); and 38 underwent transient coronary occlusion (10–40
min) followed by 48 h of reperfusion. In postmortem histological
examination of the dogs' hearts by light and electron microscopy, we
looked for ischemia or necrosis. The presence of cell swelling and
glycogen depletion was indicative of ischemia, whereas the added
presence of cell disruption indicated necrosis. Coronary
occlusion for 
20 min consistently increased plasma mitochondrial and
total CK activity and produced histologically evident myocardial
necrosis. In contrast, after 10 to 15 min of coronary occlusion, 12 of
14 animals, despite extensive severe reversible ischemia, showed no
increase in plasma CK; the remaining 2, which had increased plasma CK,
had subendocardial necrosis. Thus, cytosolic or mitochondrial CK is
released from the heart only when there has been irreversible
myocardial injury—a finding with significant diagnostic and
therapeutic implications.
Key Words: indexing terms: mitochondrial enzymes • coronary occlusion • dogs • heart damage • radioimmunoassay
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