The influence of global ischemia on myocardial nucleotide catabolite p
roduction and contraction was studied in Langendorff-perfused rat hear
ts. Hearts in the ''ischemic'' group were subjected to a 25 minute per
iod of global ischemia at 30 minutes from the start of perfusion, and
to two 30 s periods of global ischemia at 20 and 80 minutes of perfusi
on. Control hearts were subjected to three 30 s periods of ischemia at
20, 45 and 80 minutes of perfusion. Left ventricular developed pressu
re and concentrations of total nucleotide catabolites and adenosine in
the coronary effluent were measured throughout. The concentration of
nucleotide catabolites increased transiently by 2.1 +/- 0.5 mu M in th
e control group and 2.2 +/- 0.8 mu M in the ''ischemic'' group, immedi
ately after 30 s ischemia at 20 minutes; while the concentration of ad
enosine increased transiently by 0.17 +/- 0.08 mu M in the control gro
up and 0.13 +/- 0.09 mu M in the ''ischemic'' group. The next 30 s isc
hemic period in control hearts caused nucleotide catabolites to increa
se by 1.7 +/- 0.5 mu M and adenosine by 0.12 +/- 0.06 mu M. In the ''i
schemic'' group, massive purine release was observed after 25 minutes
of ischemia, the release decreasing to below pre-ischemic levels after
10 minutes of reperfusion. The increases in effluent nucleotide catab
olites and adenosine in response to 30 s ischemia at 80 minutes were 1
.4 +/- 0.4 mu M and 0.13 +/- 0.1 mu M, respectively, in the control gr
oup. In contrast, in the ''ischemic'' group, nucleotide catabolites in
creased by only 0.3 +/- 0.2 mu M and adenosine by 0.011 +/- 0.008 mu M
after 30 s ischemia at the same time. At 20 minutes of perfusion, dev
eloped pressure was 129 +/- 7 mm Hg in the ''ischemic'' group and 135
+/- 9 mm Hg in the control group. It was maintained at 116 +/- 4 in co
ntrols and recovered to 116 +/- 11 mm Hg in ischemic hearts at 80 minu
tes of perfusion. The minimum values for developed pressure during the
subsequent 30 s ischemic intervals were within the range 31-36 mm Hg,
independent of time or tbe preceding 25 minutes ischemia. These resul
ts suggest that ''retaliatory'' adenosine production is impaired in th
e heart after ischemia, which may result in increased susceptibility t
o the damaging effects of external stimulation.