Brain ischemia alters platelet ATP diphosphohydrolase and 5 '-nucleotidaseactivities in naive and preconditioned rats

The effects of transient forebrain ischemia, reperfusion and ischemic preco nditioning on rat blood platelet ATP diphosphohydrolase and 5'-nucleotidase activities were evaluated. Adult Wistar rats were submitted to 2 or 10 min of single ischemic episodes, or to 10 min of ischemia 1 day after a 2-min ischemic episode (ischemic preconditioning) by the four-vessel occlusion me thod. Rats submitted to single ischemic insults were reperfused for 60 min and for 1, 2, 5, 10 and 30 days after ischemia; preconditioned rats were re perfused for 60 min 1 and 2 days after the long ischemic episode. Brain isc hemia (2 or 10 min) inhibited ATP and ADP hydrolysis by platelet ATP diphos phohydrolase. On the other hand, AMP hydrolysis by 5'-nucleotidase was incr eased after 2, but not 10, min of ischemia. Ischemic preconditioning follow ed by 10 min of ischemia caused activation of both enzymes. Variable period s of reperfusion distinctly affected each experimental group. Enzyme activi ties returned to control levels in the 2-min group. However, the decrease i n ATP diphosphohydrolase activity was maintained up to 30 days of reperfusi on after 10-min ischemia. 5'-Nucleotidase activity was decreased 60 min and 1 day following 10-min ischemia; interestingly, enzymatic activity was inc reased after 2 and 5 days of reperfusion, and returned to control levels af ter 10 days. Ischemic preconditioning cancelled the effects of 10-min ische mia on the enzymatic activities. These results indicate that brain ischemia and ischemic preconditioning induce peripheral effects on ecto-enzymes fro m rat platelets involved in nucleotide metabolism. Thus, ATP, ADP and AMP d egradation and probably the generation of adenosine in the circulation may be altered, leading to regulation of microthrombus formation since ADP aggr egates platelets and adenosine is an inhibitor of platelet aggregation.