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1 Research Institute of Cardiology, Minsk, Belarus
2 Medicine - Cardiology, University of Minnesota, Minneapolis, MN, USA
3 National Cardiology Research Center, Moscow, Russian Federation; Research Institute of Cardiology, Minsk, Belarus
4 National Cardiology Research Center, Moscow, Russian Federation
* To whom correspondence should be addressed. E-mail: zhang047{at}umn.edu.
The myocardial ATP concentration is significantly decreased in failing hearts, which maybe related to the progressive loss of myocardial total adenine nucleotide pool (TAN). The total myocardial interstitial purine metabolites (IPM) in the dialysate of interstitial fluid could reflect the tissue ATP depletion. In rats, postinfarction (MI) left ventricular (LV) remodeling was induced by ligation of the coronary artery. Cardiac microdialysis was employed to assess changes of IPM in response to graded 
-adrenergic stimulation with isoproterenol (ISO) in myocardium of hearts with postinfarction LV remodeling (MI), or hearts with sham-operation (Sh). The dialysate samples were analyzed for adenosine (ADO), inosine, hypoxanthine, xanthine (XAN) and uric acid (UA). LV volume was greater in the MI group (2.2±0.2 ml/kg) as compared to the Sh group (1.3±0.2 ml/kg, p<0.05). Infarct size was 28±4%. Baseline dialysate level of UA was higher in MI group (18.9±3.4 µmol) as compared to Sh group (4.6±0.7µmol, p<0.01). During and after ISO infusion, the dialysate levels of ADO, XAN and UA were all significantly higher in the MI group. Thus, the level of IPM is increased in hearts with postinfarction LV remodeling both at baseline and during ISO infusion. These results suggest that the decreased myocardial ATP level in hearts with postinfarction LV remodeling may be caused by the chronic depletion of TAN.
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