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* To whom correspondence should be addressed. E-mail: rlasley{at}uky.edu.
The purpose of this study was to determine whether the adenosine A1/A2a receptor agonist AMP579 induces acute and delayed preconditioning against in vivo myocardial stunning. Regional stunning was produced by 15 minutes coronary artery occlusion and 3 hours reperfusion (RP) in anesthetized open-chest pigs. In acute protection studies, animals were pretreated with saline, low dose AMP579 (15 µg/kg, i.v. bolus 10 min before ischemia), or high dose AMP579 (50 µg/kg, i.v; 14 µg/kg bolus + 1.2 µg/kg/min for 30 min before coronary occlusion). The delayed preconditioning effects of AMP579 were evaluated 24 hours after administering saline vehicle or AMP579 (50 µg/kg, i.v.). Load-insensitive contractility was assessed by measuring regional preload recruitable stroke work (PRSW) and PRSW area (PRSWA). Acute pretreatment with AMP579 dose-dependently improved regional PRSW (129 ±5% in the high dose AMP579 group vs. 100 ± 2% in the low dose AMP579 group and 78 ± 5% in the control group at 3hr RP). Administration of the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.7 mg/kg) blocked the acute protective effect of high-dose AMP579, indicating that these effects are mediated through A1 receptor activation. Delayed preconditioning with AMP579 significantly increased the recovery of PRSWA (64 ± 5% vs. 33 ± 5% in the controls at 3hr RP). In isolated perfused rat heart studies the kinetics of the onset and washout of AMP579 A1 and A2a mediated effects were distinct compared to other adenosine receptor agonists. The unique nature of the adenosine agonist AMP579 may play a role in its ability to induce delayed preconditioning against in vivo myocardial stunning.
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