Key result
Increased adenosine formation, not substrate cycling, drives elevated adenosine during ATP catabolism in rat hearts.
Population
Rat polymorphonuclear leucocytes, cultured neonatal-rat heart cells, and isolated perfused rat hearts
Comparison
Treatment with 2'-deoxycoformycin and… vs Basal conditions or perfusion with…
Design
Preclinical
Authors
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No immediate change to adenosine modulation in ischemia; leaves open whether formation rate governs human ATP catabolism.
The study demonstrates that increased adenosine formation, rather than a substrate cycle, primarily drives elevated adenosine concentrations during ATP catabolism in rat models.
Newby et al. (1983) studied this question. 2'-deoxycoformycin, 5-iodotubercidin, hypoxic buffer, and adenosine infusion was evaluated on Rate of adenosine accumulation and formation. An increase in the rate of adenosine formation, rather than a substrate cycle, is the principal cause of elevations in adenosine concentration during ATP catabolism in rat cells and isolated hearts.