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Department of Thoracic and Cardiovascular Surgery, Kansai Medical University, Moriguchi, Osaka 570-8507, Japan
Although
adenosine is an important mediator of ischemic preconditioning
(IPC), its relative contribution to IPC remains unknown. Because
adenosine is formed through the hydrolysis of ATP, the present study
investigated the role of ATP and adenosine in IPC. Isolated and
buffer-perfused rat hearts underwent IPC by three cycles of 5-min
ischemia and 5-min reperfusion before 25 min of global
ischemia. The rate-pressure product (RPP) 30 min after reperfusion was taken as an endpoint of functional protection. Interstitial fluid (ISF) adenine nucleotides and adenosine were measured by cardiac microdialysis techniques. Inhibition of IPC-induced recovery of RPP was partial by the adenosine receptor antagonist 8-(p-sulfophenyl)theophylline (SPT; 100 µM) or by the
structurally distinct P2Y purinoceptor antagonists suramin (300 µM)
or reactive blue (RB; 10 µM) but was additive when SPT was given with
suramin or RB. The P2X antagonist
pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid tetrasodium (50 µM) had no effect on functional protection. The improved functional
recovery was not significantly affected by an ecto-5'-nucleotidase
inhibitor, 
,
-methylene adenosine diphosphate (AMP-CP; 100 µM),
alone but was inhibited by AMP-CP plus SPT, suramin, or RB. ISF
ATP and adenosine increased temporarily by 10-fold during IPC. AMP-CP
augmented the increase in ISF ATP associated with the decrease in ISF
adenosine. There was a reciprocal correlation between the ISF
concentration of ATP and adenosine in preconditioned hearts. In
addition, there was a significant correlation between ISF adenosine and
ATP and the inhibitory potency of SPT and suramin or RB against
functional protection conferred by IPC. These results suggest that
extracellular ATP and adenosine play a complementary role in IPC
through P2Y purinoceptors and adenosine receptors, respectively.
cardiac microdialysis
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