Why the study?
Does beta-adrenergic stimulation with isoproterenol increase interstitial purine metabolites in rats with post-MI LV remodeling compared to sham-operated rats?
Does beta-adrenergic stimulation with isoproterenol increase interstitial purine metabolites in rats with post-MI LV remodeling compared to sham-operated rats?
In a rat model of post-MI LV remodeling, interstitial purine metabolites are increased at baseline and during beta-adrenergic stimulation, suggesting chronic depletion of the total adenine nucleotide pool causes decreased myocardial ATP.
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Hypothesis-generating for adenine nucleotide depletion in post-MI remodeling; leaves open translational relevance pending further animal and human studies.
The myocardial ATP concentration is significantly decreased in failing hearts, which may be related to the progressive loss of the myocardial total adenine nucleotide pool. The total myocardial interstitial purine metabolites (IPM) in the dialysate of interstitial fluid could reflect the tissue ATP depletion. In rats, postmyocardial infarction (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 beta-adrenergic stimulation with isoproterenol (Iso) in myocardium of hearts with post-MI LV remodeling (MI group) or hearts with sham operation (sham group). The dialysate samples were analyzed for adenosine, inosine, hypoxanthine, xanthine, and uric acid. LV volume was greater in the MI group (2.2 +/- 0.2 ml/kg) compared with the sham group (1.3 +/- 0.2 ml/kg, P < 0.05). Infarct size was 28 +/- 4%. The baseline dialysate level of uric acid was higher in the MI group (18.9 +/- 3.4 micromol) compared with the sham group (4.6 +/- 0.7 micromol, P < 0.01). During and after Iso infusion, the dialysate levels of adenosine, xanthine, and uric acid 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 post-MI LV remodeling may be caused by the chronic depletion of the total adenine nucleotide pool.
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Gourine et al. (2004) studied this question.
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