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Myocardial protection in beating heart cardiac surgery: I: Pre-or postconditioning with inhibition of es-ENT1 nucleoside transporter and adenosine deaminase ...

AS Abd-Elfattah, H Aly, S Hanan... - The Journal of Thoracic ..., 2012 - Elsevier Objective To determine the role of the p-nitrobenzylthioinosine-sensitive equilibrative nucleoside transporter 1 (es-ENT1) in postmyocardial infarction reperfusion injury-mediated ventricular fibrillation and regional dysfunction. We used erythro-9 (2-hydroxy-3-nonyl)- ... [CITATION] 143 Logistic Euro SCORE by longitudinal global strain in predicting outcome after cardiac surgery M Berry, J Nahum, O Zaghden, JL Monin... - Archives of ..., 2012 - Elsevier

Figure E1. Role of adenine nucleosides metabolism and transport by way of es-NT1 (compartmentalization) in purine-mediated post-myocardial infarction reperfusion injury. The figure illustrates purine metabolism and compartmentalization in relation to ischemic and reperfusion injury in the untreated control group (A). Ischemia is associated with intracellular adenosine triphosphate (ATP) depletion. Sympathetic stimulation at the onset of ischemia results in neurotransmitter and ATP co-release, elevating extracellular ATP. Ecto- and endo-5 -nucleotidase (endo) and adenosine deaminase continue breaking down ATP and adenosine monophosphate (AMP) during ischemia to adenosine in the intracellular and extracellular compartments. Adenosine is rapidly deaminated to inosine by adenosine deaminase. Extracellular inosine is converted by inosine phosphorylase (IP Lase) to hypoxanthine, and the latter is oxidized to xanthine and superoxide radicals during cardiac ischemia and reperfusion. Intracellular inosine and the remaining adenosine are rapidly released on reperfusion by way of the p-nitrobenzylthioinosine (NBMPR)-sensitive adenine nucleoside transporter-1 (es-ENT1), allowing abrupt formation of hypoxanthine, xanthine, and free radicals. The effect of preischemic treatment with EHNA/NBMPR of purine metabolism and compartmentalization is depicted in part B. Adenosine is maintained inside and outside cells. C, Effect of MI postconditioning with EHNA/NBMPR. Intracellular inosine is the major end product of ATP depletion during ischemia. Similar to the control group, noncardiac ATP is broken down to xanthine, producing free radicals in the circulation. Infusion of EHNA/NBMPR after MI but before releasing the left anterior descending coronary artery occlusion allowed entrapment of intracellular inosine, limiting the reperfusion injury mediated by free radicals. ADP, Adenosine diphosphate; AMP, adenosine monophosphate; ecto-5 NT Dase, 5 -nucleotidase; es-ENT1, equilibrative p-nitro-benzylthioinosine (NBMPR)-sensitive adenine nucleoside transport 1; A1R, adenosine receptor 1; IP Lase, inosine phosphorylase; XO, xanthine oxidase; O2, molecular oxygen; .O 2, superoxide radical. The font size reflects the amount of purine at ischemia or reperfusion.