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1 Critical Care Medicine, St. Jude Children's Research Hospital, Memphis, Tennessee, United States
2 Physiology & Pharmacology, West Virginia University, Morgantown, West Virginia, United States
3 Durham Research Center, University of Nebraska Medical Center, Omaha, Nebraska, United States
4 Physiology, 6N-98 Brody, ECU School of Medicine, Greenville, North Carolina, United States
5 Building 10, Room 4 D51, NIDDK, NIH, Bethesda, Maryland, United States
* To whom correspondence should be addressed. E-mail: ray.morrison{at}stjude.org.
To examine ischemic tolerance in the absence of A1 adenosine receptors (A1ARs), isolated wild-type (WT) and A1AR knockout (A1KO) murine hearts underwent global ischemia-reperfusion, and injury was measured in terms of functional recovery and efflux of lactate dehydrogenase (LDH). Hearts were analyzed by real-time RT-PCR both at baseline and at intervals during ischemia-reperfusion to determine whether compensatory expression of other adenosine receptor subtypes occurs with either A1AR deletion and/or ischemia-reperfusion. A1KO hearts had higher baseline coronary flow (CF) and left ventricular developed pressure (LVDP) than WT hearts, while heart rate was unchanged by A1AR deletion. Following 20 min ischemia, CF was attenuated in A1KO compared to WT hearts and this reduction persisted throughout reperfusion. Final recovery of LVDP was decreased in A1KO hearts (54.4±5.1 v. WT 81.1±3.4 % pre-ischemic baseline), and correlated with higher diastolic pressure during reperfusion. Post-ischemic efflux of LDH was greater in A1KO compared to WT hearts. Real-time RT-PCR demonstrated absence of A1AR transcript in A1KO hearts, and the message for A2A, A2B and A3 adenosine receptors was similar in un-instrumented A1KO and WT hearts. Ischemia-reperfusion increased A2B mRNA expression 2.5-fold in both WT and A1KO hearts without changing A1 or A3 expression. In WT hearts, ischemia transiently doubled A2A mRNA which returned to pre-ischemic level upon reperfusion, a pattern not observed in A1KO hearts. Together, these data affirm the cardioprotective role of A1ARs, and suggest that induced expression of other adenosine receptor subtypes may participate in the response to ischemia-reperfusion in isolated murine hearts.
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