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
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Cite this
Kaplan, L. J., Bellows, C. F., Carter, S., Blum, H., & Whitman, G. J. R. (1995). The phosphocreatine overshoot occurs independent of myocardial work. Biochimie, 77(4), 245-248. https://doi.org/10.1016/0300-9084(96)88131-4