D, Effects of a hot shot and reperfusion with EHNA/NBMPR before and after continuous retrograde coronary sinus hypothermic cardioplegia on myocardial total diffusible purines (adenosine + inosine + hypoxanthine + xanthine) of the left ventricle in acutely ischemic hearts. C, Effects of a hot shot and reperfusion with EHNA/NBMPR, before and after continuous retrograde coronary sinus hypothermic cardioplegia, on myocardial inosine of the left ventricle in acutely ischemic hearts. B, Effects of a hot shot and reperfusion with EHNA/ NBMPR before and after continuous retrograde coronary sinus hypothermic cardioplegia on myocardial adenosine of the left ventricle in acutely ischemic hearts. A, Effects of a coronary sinus hot shot and reperfusion with EHNA/NBMPR before and after continuous retrograde coronary sinus hypothermic cardioplegia on myocardial ATP of the left ventricle in acutely ischemic hearts. The P value was not significant among groups using analysis of variance. All hearts were subjected to 20 minutes of warm aortic crossclamping on-pump, a hot shot with or without EHNA/NBMPR, followed 100 minutes of retrograde hypothermic cardioplegic arrest and 60 minutes of reperfusion with or without inhibitors. Inhibition of cardiac es-ENT1 nucleoside transporter abolishes postischemic reperfusion injury in warm and cold cardiac surgery.ДЎ6 17 18 31 ATP EHNA HPLC NBMPR adenosine triphosphate equilibrative-p-nitrobenzylthioinosineвЂ“sensitive type of the equilibrative nucleoside transport 1 erythro-9-adenine es-ENT1 high-performance liquid chromatography p-nitrobenzylthioinosine.Д®ffects of a coronary sinus hot shot and reperfusion with EHNA/NBMPR before and after continuous retrograde coronary sinus hypothermic cardioplegia on myocardial ATP pool metabolism of the left ventricle in acutely ischemic hearts. Induction of hypothermic cardioplegia releases purines from ischemic hearts until they become cold, whereas reperfusion induces massive purine release and myocardial stunning. Reperfusion with EHNA/NBMPR abolished ventricular dysfunction in acutely ischemic hearts with and without a hot shot and hypothermic cardioplegic arrest.

Induction of intermittent antegrade or continuous retrograde hypothermic (4вЊ) cardioplegia releases purines until the heart becomes cold (90% of purines in coronary sinus effluent. Warm ischemia depleted myocardial adenosine triphosphate and elevated purines (ie, inosine > adenosine) as markers of ischemia. Myocardial biopsies and coronary sinus effluents were obtained and analyzed using high-performance liquid chromatography. It is not known whether prolonged administration of hypothermic cardioplegia influences purine release and EHNA/NBMPR-mediated cardioprotection in acutely ischemic hearts.ДЄnesthetized dogs (n = 46), which underwent normothermic aortic crossclamping for 20 minutes on-pump, were divided to determine (1) purine release with induction of intermittent antegrade or continuous retrograde hypothermic cardioplegia and reperfusion, (2) the effects of postischemic treatment with 100 ОјM EHNA and 25 ОјM NBMPR on purine release and global functional recovery, and (3) whether a hot shot and reperfusion with EHNA/NBMPR inhibits purine release and attenuates ventricular dysfunction of ischemic hearts. Simultaneous inhibition of the cardiac equilibrative-p-nitrobenzylthioinosine (NBMPR)-sensitive (es) type of the equilibrative nucleoside transport 1 (ENT1) nucleoside transporter, with NBMPR, and adenosine deaminase, with erythro-9-adenine (EHNA), prevents release of myocardial purines and attenuates myocardial stunning and fibrillation in canine models of warm ischemia and reperfusion.

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