Intracellular compartmentation of troponin T: release kinetics after global ischemia and calcium paradox in the isolated perfused rat heart
A. Remppis, T. Scheffold, J. Greten, M. Haas, T. Greten, W. Kübler and H. A. Katus. Intracellular Compartmentation of Troponin T: Release Kinetics After Global Ischemia and Calcium Paradox in the Perfused Rat Heart. Journal of Molecular and Cellular Cardiology (1995) 27, 793-803. The marked differe...
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| Main Authors: | , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
February 1995
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| In: |
Journal of molecular and cellular cardiology
Year: 1995, Volume: 27, Issue: 2, Pages: 793-803 |
| ISSN: | 1095-8584 |
| DOI: | 10.1016/0022-2828(95)90086-1 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/0022-2828(95)90086-1 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/0022282895900861 
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| Author Notes: | Andrew Remppis, Thomas Scheffold, Johannes Greten, Markus Haass, Tobias Greten, Wolfgang Kübler, Hugo A. Katus |
MARC
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| 245 | 1 | 0 | |a Intracellular compartmentation of troponin T |b release kinetics after global ischemia and calcium paradox in the isolated perfused rat heart |c Andrew Remppis, Thomas Scheffold, Johannes Greten, Markus Haass, Tobias Greten, Wolfgang Kübler, Hugo A. Katus |
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| 520 | |a A. Remppis, T. Scheffold, J. Greten, M. Haas, T. Greten, W. Kübler and H. A. Katus. Intracellular Compartmentation of Troponin T: Release Kinetics After Global Ischemia and Calcium Paradox in the Perfused Rat Heart. Journal of Molecular and Cellular Cardiology (1995) 27, 793-803. The marked differences in troponin T serum concentrations observed in patients with reperfused and non-reperfused myocardial infarction may be due to a perfusion dependent wash-out of an unbound fraction of cardiac troponin T. To test the release kinetics of troponin T experimentally, the isolated rat heart (Langendorff preparation) was damaged either by the calcium paradox or by no-flow ischemia. Following membrane damage by the calcium paradox troponin T (TNT) showed the same release kinetics in the coronary effluent as the cytosolic markers creatine kinase (CK) or lactate dehydrogenase (LDH). Peak levels of troponin T (282 ± 58 μg/l), CK (6754 ± 1642 U/l), and LDH (5817 ± 1730 U/l) occurred 5 min after onset of reperfusion with calcium containing buffers and returned to 9.9%, 1.3%, and 1% of their respective peak levels within 55 min of reperfusion. During reperfusion after no-flow ischemia different release kinetics were found for cytosolic enzymes and troponin T. After 60 min of ischemia, troponin T levels in the coronary effluent increased over the entire reperfusion period of 55 min, almost doubling the 5 min value (191%). In contrast, cardiac enzymes rapidly declined to 18% (CK) and 23% (LDH) of their respective 5 min values at the end of reperfusion. Light microscopy after reperfusion with carbon black revealed a complete and homogenous reperfusion of Langendorff hearts after no-flow ischemia. Immunoblot analysis confirmed the release of an undegraded 39 kDa troponin T molecule, both after global ischemia and the calcium paradox. These data indicate that prolonged ischemia induces a continuous liberation of cardiac troponin T, most probably from disintegrating myofibres, whereas membrane damage leads almost exclusively to leakage of a functionally unbound troponin T pool. These findings may explain the biphasic serum concentration changes of cardiac troponin T in patients with reperfused myocardial infarction. | ||
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| 650 | 4 | |a Reperfusion | |
| 650 | 4 | |a Troponin T | |
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