Direct measurements of intracellular free Ca2+ concentration ([Ca2+](i)) were obtained during ischemia and reperfusion in ferret hearts loaded with the Ca2+ indicator, the 5,5'-difluoro derivative of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N',-tetraacetic acid. During 15 minutes of ischemia at 37°C, time-averaged [Ca2+](i) increased significantly and rapidly during reperfusion. In contrast to metabolic inhibition in isolated muscle or cells, the increase in [Ca2+](i) during true ischemia occurs in the absence of a mechanical contracture. After ischemia, contractile function does not recover completely: the hearts are 'stunned'. Our results support the hypothesis that an increase in cellular calcium-loading causes dysfunction in the form of myocardial stunning while leaving unresolved the precise mechanism of the calcium-mediated injury.
|Original language||English (US)|
|Issue number||6 SUPPL.|
|State||Published - Dec 1 1989|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)