Abstract
Although the exact mechanism(s) responsible for the phosphocreatine/ATP overshoot have not been completely elucidated, our data demonstrate that the overshoot does not stem from reduced myocardial work, and consequently, reduced utilization of phosphocreatine (PCr). Additionally, we highlight a basic difference in the physiologic responses of skeletal and cardial muscle to work demands. By understanding the bioenergetic derangements which accompany reperfusion injury, one may hope to better salvage post-ischemic myocardium.
Original language | English (US) |
---|---|
Pages (from-to) | 245-248 |
Number of pages | 4 |
Journal | Biochimie |
Volume | 77 |
Issue number | 4 |
DOIs | |
State | Published - 1995 |
Externally published | Yes |
Keywords
- myocardial work
- phosphocreatine overshoot
- post-ischemic myocardium
ASJC Scopus subject areas
- Biochemistry