1. Cardiac release of urocortin precedes the occurrence of irreversible myocardial damage in the rat heart exposed to ischemia/reperfusion injury
- Author
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Roy B. McCauley, Paul A. Townsend, Alessandro Mazzucco, David S. Latchman, Tiziano M. Scarabelli, Louis D. Saravolatz, Hardial S. Chowdrey, Gabriele Scarabelli, Giuseppe Faggian, J. Di Rezze, Zhaokan Yuan, Anastasis Stephanou, Carol Chen-Scarabelli, and Richard A. Knight
- Subjects
Male ,Programmed cell death ,medicine.medical_specialty ,endocrine system ,Necrosis ,Biophysics ,Ischemia ,Myocardial Reperfusion Injury ,Apoptosis ,Biochemistry ,Rats, Sprague-Dawley ,Structural Biology ,Internal medicine ,Genetics ,medicine ,Animals ,Myocyte ,Molecular Biology ,Urocortins ,Urocortin ,business.industry ,Cell Biology ,Rat heart ,Biomarker ,medicine.disease ,Sublethal ischemia ,Rats ,Endocrinology ,medicine.symptom ,business ,Reperfusion injury ,Biomarkers ,hormones, hormone substitutes, and hormone antagonists - Abstract
This study evaluates whether cardiac ischemia induces release of urocortin, before and independently from myocyte cell death. Urocortin levels rose after 5-min ischemia and peaked after 10-min ischemia, when cell death was not detected. However, myocyte apoptosis and/or necrosis occurred following 20- and 30-min ischemia, which paralleled a fall in urocortin levels, suggesting that urocortin expression and release are mainly sustained by metabolically challenged, though still viable myocytes. Hence, since cardiac release of urocortin, unlike that of conventional biomarkers, occurs before and apart from cell death, urocortin levels may be clinically useful in the diagnosis of sublethal myocardial ischemia.
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