Release of nucleosides from canine and human hearts as an index of prior ischemia

Fox, Arthur C.; Reed, George E.; Meilman, Henry; Silk, Barbara B.

doi:10.1016/0002-9149(79)90044-4

Cited by 94 publications

(25 citation statements)

References 25 publications

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“…21,22) Elevated serum UA levels might reflect impaired oxidative metabolism by xanthine oxidase activity, since tissue hypoxia and cell death deplete adenosine triphosphate with degradation of adenosine nucleotides to compounds including UA. 23,24) In addition to oxidative metabolism, an increase in serum UA concentrations is a marker of inflammatory cytokine activation and impaired vascular function in various cardiovascular diseases. 25,26) Additionally, several recent studies have revealed that oxidative stress decreased with epoprostenol therapy in PAH patients.…”

Section: Discussionsupporting

confidence: 59%

Serum Uric Acid as a Prognostic Predictor in Pulmonary Arterial Hypertension With Connective Tissue Disease

et al. 2007

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SUMMARYBackground: Pulmonary arterial hypertension (PAH) has been identified as a life threatening complication of connective tissue disease. However, the association between serum uric acid (UA) levels and long-term outcome in PAH with connective tissue disease has not been evaluated. We therefore assessed whether serum UA levels are related to the mortality of such patients. Methods and results:We investigated 90 consecutive patients with connective tissue disease who were initially diagnosed with PAH by echocardiography, and assessed the long-term clinical outcome in populations with higher (≥ 4.7 mg/dL) and lower serum UA levels. Kaplan-Meier analysis showed that patients with higher median serum UA values had a significantly worse survival rate for any cause of death (54.5% versus 84.7%, logrank, P < 0.01) and PAH-related death (72.7% versus 93.4%, log-rank, P < 0.01) than those with low values. Multivariate analysis showed that an elevated serum UA level was an independent predictor for survival (hazard ratio, 1.88, 95% CI [1.24-2.84], P < 0.01). Conclusion:Elevated serum UA levels are associated with a poor prognosis and can serve as a prognostic predictor for patients with PAH secondary to connective tissue disease. (Int Heart J 2007; 48: 523-532)

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Section: Discussionsupporting

confidence: 59%

Serum Uric Acid as a Prognostic Predictor in Pulmonary Arterial Hypertension With Connective Tissue Disease

et al. 2007

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“…The results of this study suggest that even brief (15 min) periods of ischemia followed by reperfusion in which no necrosis occurs as assessed both histologically and histochemically (100% salvage) result in abnormalities of myocardial biochemistry, function, and ultrastructure which require up to 7 days for complete recovery. One possible explanation for prolonged recovery of ATP is that precursors necessary for ATP resynthesis are washed out ofthe ischemic myocardium during reperfusion (10). Whether prolonged recovery of systolic function is due to decreased ATP or to a primary abnormality in calcium metabolism remains controversial (11,12).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Recovery from prolonged abnormalities of canine myocardium salvaged from ischemic necrosis by coronary reperfusion.

Kloner¹,

DeBoer²,

Darsee³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

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The purpose of this study was to determine whether or not the biochemical, functional, and ultrastructural abnormalities produced by brief temporary coronary occlusions (unassociated with necrosis) ever resolve and, if so, when they do. Anesthetized open-chest dogs were subjected to 15 min ofcoronary artery occlusion followed by 72 hr, 7 days, or 14 days of reperfusion. Serial in vivo myocardial biopsies were performed for measurement of ATP and for ultrastructural analysis. Regional function was evaluated by sonomicrometry. Mean (±SEM) my-

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“…However, one observation suggested that the basis of this prolonged post anoxic/ischemic ATP depletion was via the loss of ATP precursors from the heart and into the perfusate or blood stream [38] (similar observations were being made by Robert Berne around the same time [39]). The importance of this loss of precursors, which also occurs in man [40], stems from the fact that the heart predominately utilises the purine salvage pathway (Fig. 1) for the resynthesis of adenine nucleotides [39].…”

Section: Basis For Atp Depletionmentioning

confidence: 99%

The Purine Salvage Pathway and the Restoration of Cerebral ATP: Implications for Brain Slice Physiology and Brain Injury

Frenguelli

2017

Neurochem Res

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Brain slices have been the workhorse for many neuroscience labs since the pioneering work of Henry McIlwain in the 1950s. Their utility is undisputed and their acceptance as appropriate models for the central nervous system is widespread, if not universal. However, the skeleton in the closet is that ATP levels in brain slices are lower than those found in vivo, which may have important implications for cellular physiology and plasticity. Far from this being a disadvantage, the ATP-impoverished slice can serve as a useful and experimentally-tractable surrogate for the injured brain, which experiences similar depletion of cellular ATP. We have shown that the restoration of cellular ATP in brain slices to in vivo values is possible with a simple combination of d-ribose and adenine (RibAde), two substrates for ATP synthesis. Restoration of ATP in slices to physiological levels has implications for synaptic transmission and plasticity, whilst in the injured brain in vivo RibAde shows encouraging positive results. Given that ribose, adenine, and a third compound, allopurinol, are all separately in use in man, their combined application after acute brain injury, in accelerating ATP synthesis and increasing the reservoir of the neuroprotective metabolite, adenosine, may help reduce the morbidity associated with stroke and traumatic brain injury.

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Release of nucleosides from canine and human hearts as an index of prior ischemia

Cited by 94 publications

References 25 publications

Serum Uric Acid as a Prognostic Predictor in Pulmonary Arterial Hypertension With Connective Tissue Disease

Serum Uric Acid as a Prognostic Predictor in Pulmonary Arterial Hypertension With Connective Tissue Disease

RETRACTED: Recovery from prolonged abnormalities of canine myocardium salvaged from ischemic necrosis by coronary reperfusion.

The Purine Salvage Pathway and the Restoration of Cerebral ATP: Implications for Brain Slice Physiology and Brain Injury

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