Isolated working rat heart preparations were used to ascertain whether the addition of
adenosine and prevention of its catabolism could aid in the functional recovery of hearts following global
ischemia. Hearts were infused with either 80 micro M
EHNA (an
adenosine deaminase inhibitor) or 20 micro M
adenosine and
EHNA in either normal (2.4 mM) or low (0.05 mM)
calcium-containing
buffer prior to clamping of the aorta for 30 minutes. In one series of hearts, postischemic concentrations (mumoles/gram wet weight) of
adenosine triphosphate (
ATP),
diphosphate (
ADP), and monophosphate (
AMP),
adenosine,
inosine, and
hypoxanthine were measured; in another series, the recovery of aortic flow rate was used as a measure of functional recovery of ventricular muscle. With normal electrolyte balance,
EHNA was unable to protect hearts against
ATP loss and ventricular failure. Hearts with
EHNA +
adenosine recovered 14% of preischemic aortic output and
ATP levels were slightly elevated at 0.93 mumole/gm. Those treated with either
EHNA or
EHNA +
adenosine in low-
calcium buffer recoverd 100% of their original aortic output. However,
EHNA +
adenosine maintained considerably higher
ATP levels (1.57 mumoles/gm) than did
EHNA alone (1.14 mumoles/gm) and was associated with faster initial recovery of aortic output. Thus the prevention of
adenosine catabolism was insufficient for adequate ventricular recovery unless the tissue
ATP was maintained above about 1.0 mumole/gm.
EHNA +
adenosine in a 0.05 mM Ca++ infusion
solution conserved
ATP, markedly improved the functional recovery of hearts, and thus may have a role to play in myocardial preservation during elective
cardiac arrest.