Arresting the heart with cardioplegia solution is the usual strategy to protect
the myocardium during cardiac surgery. However, ischemia-reperfusion injury,
due in part to Ca2+ overload, remains a clinical problem. Ca2+ influx during
ischemia occurs through reverse mode action of the Na+/Ca2+ exchanger. We
therefore tested the hypothesis that delivering the Na+/Ca2+ exchanger blocker
SEA0400 to a cardioplegia solution would result in superior myocardial protection
during ischemic-cardioplegic arrest. Studies were performed on isolated hearts
and individual cardiomyocytes from young adult male Fisher Rats. Hearts
arrested with cardioplegia containing SEA0400 showed improved recovery of left
ventricular function after reperfusion. The onset of reperfusion arrhythmia was
delayed, troponin release was reduced, and mitochondrial damage was
minimized. In the isolated cell model, contraction amplitudes were higher during
reperfusion in the SEA0400 group without a change in Ca2+ transients. This
suggests that cells arrested with cardioplegia containing SEA0400 developed
improved myofilament sensitivity to Ca2+.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:NSHD.ca#10222/14254 |
| Date | 13 May 2011 |
| Creators | Ali, Ahmad |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
Page generated in 0.0017 seconds