DEPRESSED ADENOSINE AND TOTAL PURINE CATABOLITE PRODUCTION IN THE POSTISCHEMIC RAT-HEART

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.