AJP - Heart and Circulatory Physiology, Vol 248, Issue 5 644-H651, Copyright © 1985 by American Physiological Society
Myocardial adenine pool depletion and recovery of mechanical function following ischemia
S. M. Humphrey, D. G. Holliss and R. N. Seelye
The loss of nucleotide pool precursors from the heart during ischemia and
reperfusion may affect resynthesis of ATP and consequently mechanical
recovery. Isolated working rat hearts were made globally ischemic for from
15 to 25 min, and the tissue content of adenine pool metabolites, creatine,
creatine phosphate (CP), and inorganic phosphate (Pi), were measured after
20 min of reperfusion. In addition, the coronary effluent was assayed for
nucleotides, nucleosides, and oxypurines. Hearts that recovered 75% or more
of their preischemic hemodynamic function had significantly lower ATP and
NAD but greater CP and Pi than controls. Complete failure of hearts was
associated with severely depleted ATP but not CP. All hearts released 25%
or more of their preischemic adenine pool during the 20-min reperfusion.
This loss correlated more closely with a reduction in recovery from 100 to
75% than with complete failure. Thus extensive loss of adenine pool
precursors is not critically related to the failure of heart muscle to
recover function but may be an important limiting factor in determining the
extent and time course of mechanical recovery.
