This article is part of the supplement: 20th International Symposium on Intensive Care and Emergency Medicine
Relationship between cardiac troponin I (cTnI) release during cardiac operations and myocardial cell death
1 Department. of Cardiac Surgery, Aachen University of Technology, Pauwelsstrasse. 30, D-52057, Aachen, Germany
2 Pediatric Cardiology, Aachen University of Technology, Pauwelsstrasse. 30, D-52057, Aachen, Germany
3 Pathology, Aachen University of Technology, Pauwelsstrasse. 30, D-52057, Aachen, Germany
Critical Care 2000, 4(Suppl 1):P2 doi:10.1186/cc722
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| Published: | 21 March 2000 |
© 2000 Current Science Ltd
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Aims
To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery.
Methods
Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy.
Results
In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1 ± 2.6 ng/ml) (mean ± SEM), CS (19.5 ± 3.2 ng/ml) and CL (5202 ± 2500 ng/ml). Percentage of total myocardial cell death was 3.1 ± 0.5%, including 1.2 ± 0.35% necrosis and 1.9 ± 0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis.
Conclusion
Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.