Urate production by human heart

Abstract

Xanthine oxidoreductase has been demonstrated in the heart of various species. However, its presence in human heart is still debated. In the literature, high to undetectable levels have been reported. We studied the arterial-venous mate difference across the heart of patients undergoing both routine cardiac catheterization and percutaneous transluminal coronary angioplasty. Urate is the end product of the reaction catalysed by xanthine oxidoreductase. In 10 patients, studied before angioplasty, the plasma mate level in the great cardiac vein exceeded the arterial one by 26 + 10 nmol/ml (P = 0.028). In a further 13 patients, urate production was maximal immediately after the last of four consecutive occlusions (23 If: 8 nmol/ml, P = 0.018) and concomitant with increased coronary sinus hypoxanthine levels. We conclude that xanthine oxidoreductase is probably present in the heart of patients, suffering from ischemic heart disease, and responsible for the increase in mate production during transient myocardial ischemia.

Serum Uric Acid Level Increases in Proportion to the Severity of Pulmonary Thromboembolism.

“…Measurement of serum UA can be repeatedly performed because it is simple, noninvasive, relatively inexpensive and routinely available. Interestingly, serum UA level in coronary sinus blood has been shown to increase following balloon inflation and to decrease following balloon deflation during coronary angioplasty, within a few minutes, 34 which does not conflict with the finding that in the present study serum UA level on admission in patients with acute PTE was already elevated soon after the onset of PTE. Thus, serum UA level may be used as a sensitive marker for the efficacy of treatment of PTE.…”

Absence of beneficial effect of intravenous metoprolol given during angioplasty in patients with single-vessel coronary artery disease

“…After ischemia, the human heart releases hypoxanthine due to A T P catabolism [14,18,[28][29][30]. In contrast to earlier work [14,30], coronary occlusion did not influence venous hypoxanthine.…”

“…The appearance of urate indicates that human heart contains some xanthine oxidoreductase activity [29]. On the other hand, perfusion of explanted human hearts with hypoxanthine gives rise to negligible urate production [32].…”

Uric acid in chronic heart failure: a marker of chronic inflammation

“…Regional ischaemia, such as that produced during coronary angioplasty [67] or tourniquet exsanguination of the forearm [68] also produces elevations in serum uric acid. We have previously shown that in chronic heart failure, serum uric acid is inversely related to maximal oxygen consumption during a maximal treadmill exercise test [1] and to maximal leg blood flow [69] .…”