Depressed adenosine and total purine catabolite production in the postischemic rat heart.

The influence of global ischemia on myocardial nucleotide catabolite production and contraction was studied in Langendorff-perfused rat hearts. Hearts in the "ischemic" group were subjected to a 25 minute period 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 perfusion. Control hearts were subjected to three 30 s periods of ischemia at 20, 45 and 80 minutes of perfusion. Left ventricular developed pressure 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 microM in the control group and 2.2 +/- 0.8 microM in the "ischemic" group, immediately after 30 s ischemia at 20 minutes; while the concentration of adenosine increased transiently by 0.17 +/- 0.08 microM in the control group and 0.13 +/- 0.09 microM in the "ischemic" group. The next 30 s ischemic period in control hearts caused nucleotide catabolites to increase by 1.7 +/- 0.5 microM and adenosine by 0.12 +/- 0.06 microM. In the "ischemic" 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 catabolites and adenosine in response to 30 s ischemia at 80 minutes were 1.4 +/- 0.4 microM and 0.13 +/- 0.1 microM, respectively, in the control group. In contrast, in the "ischemic" group, nucleotide catabolites increased by only 0.3 +/- 0.2 microM and adenosine by 0.011 +/- 0.008 microM after 30 s ischemia at the same time.(ABSTRACT TRUNCATED AT 250 WORDS)