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Articles in PresS, published online ahead of print August 8, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00209.2002
Submitted on March 11, 2002
Accepted on July 22, 2002
1 Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan
2 Division of Cardiology, University of Louisville and Jewish Hospital Heart and Lung Institute, Louisville, KY, USA
* To whom correspondence should be addressed. E-mail: shimmura{at}sc.itc.keio.ac.jp.
Opioids confer biphasic (early and late) cardioprotection against myocardial infarction by opening mitochondrial KATP channels. It is unknown whether cyclooxygenase-2 (COX-2), which mediates ischemia-induced late preconditioning, also mediates opioidinduced cardioprotection. Isolated perfused rat hearts were subjected to 20 min of global ischemia followed by 20 min of reperfusion. BW373U86 (BW), a 
-opioid receptor agonist, was administered 1, 12, or 24 h before sacrifice. The recovery of left ventricular developed pressure (LVDP) after ischemia/reperfusion improved when BW was administered 1 or 24 h before ischemia (control: 57±8, BW 1 h: 75±5, BW 24 h: 85±6%) but not when it was administered 12 h before (60±5%). The levels of 6-keto-PGF1
(a stable metabolite of PGI2) in coronary effluent after 20 min of reperfusion were higher with 24-h BW pretreatment than in controls (1053±92 vs. 724±81 pg/mL), whereas 6-keto- PGF1 levels at baseline did not differ. Administration of a selective COX-2 inhibitor, NS-398, abolished the late phase of cardioprotection (recovery of LVDP, 53±8%) and attenuated the increase in PGI2 (706±138 pg/mL) but did not block the early phase of cardioprotection. The selective COX-1 inhibitor, SC-560, did not affect either phase of protection. Western immunoblotting revealed upregulation of PGI2 synthase protein 24 h after BW administration without changes in COX-1 and COX-2 protein levels. In conclusion, the late (but not the early) phase of -opioid receptor-induced preconditioning is mediated by COX-2. A functional coupling between COX-2 and upregulated PGI2 synthase appears to underlie this cardioprotective phenomenon in the rat.
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