Effect of uridine supply on glycogen resynthesis after ischaemia in the isolated perfused rat heart

Abstract

Isolated rat hearts were subjected to 30 min low flow ischaemia (0.5 ml X min-1). During reperfusion, uridine (5 X 10(-5) mol X litre-1) was added to the perfusion medium for 30 min. The concentrations of creatine phosphate, adenine nucleotides, uridylic nucleotides and glycogen were determined at the end of the experiments. The purpose of this work was to study the effects of uridine supply on the concentration of energetic compounds during reperfusion recovery. Low flow ischaemia induced a breakdown of creatine phosphate, adenosine triphosphate, and total adenine nucleotides by 53%, 23% and 15% respectively. The creatine phosphate content was restored during reperfusion without uridine, but the adenine nucleotides remained unchanged. The uridylic nucleotides and the glycogen were also degraded during ischaemia by 56% and 53% for uridine triphosphate and glycogen respectively. Reperfusion without uridine induced a partial resynthetisation of uridylic nucleotides but glycogen stores were not significantly restored. When tested in oxygenated hearts, uridine supply induced a fall in creatine phosphate concentration and an enhancement of uridine triphosphate level but it had no effect on adenosine triphosphate, uridine diphosphate glucose or glycogen concentrations. If supplied during reperfusion, the nucleoside induced the complete restoration of myocardial ATP, total adenine nucleotide content, an increase in the uridylic nucleotide concentration and the resynthetisation of glycogen to supra-normal value.

Uridine Protects Cortical Neurons from Glucose Deprivation-Induced Death: Possible Role of Uridine Phosphorylase

“…In other reports using the heart and brain, researchers employed uridine by the perfusion and intraperitoneal injection, respectively (Benzi et al, 1984;Aussedat, 1983;Geiger and Yamasaki, 1954;Sapronov et al, 2000). The present study used another way for determining the uridine effect in in vivo model and revealed orally administrated uridine reduced the MCAO/reperfusion-induced brain damage.…”

“…Therefore, it is possible that, as in the case of purine nucleosides, uridine may increase cell survival under ischemic insults through the action of UPase. In fact, uridine has been thought to be an alternative energy source in rat heart and brain during ischemic situations even though UPase's role for this has not been revealed yet (Geiger and Yamasaki, 1954;Aussedat, 1983;Benzi et al, 1984;Sapronov et al, 2000). Moreover, based on our previous finding, it is obvious that uridine blocks the ischemiclike insult-evoked death of astrocytes by preserving cellular ATP levels and in this scheme, UPase is involved (Choi et al, 2006).…”

Changes in cardiac glycogen synthase and phosphorylase activities following stimulation of beta-adrenergic receptors in rats

“…are used fast depletion of glycogen also occurs but the restoration is faster and a large "supercompensation" (200 %) several hours following isoprenaline injection was shown by Towart et al (20). Since the restoration of glycogen could be accelerated by increasing the synthesis of uracil nucleotides via uridine supply, we suggested that resynthesis of cardiac glycogen could be in part limited by the actual intracellular concentration of UDPG (uridine diphosphoglucose): the substrate of the ultimate step of glycogen synthesis (3,2).…”

Energy metabolism response to calcium activation in isolated rat hearts during development and regression of T3-induced hypertrophy

“…The adenine nucleotide contents were measured using a previously described HPLC method [22]. Briefly, the column used was a Partisil-10-ODS-2-Whatman, the mobile phase was sodium pyrophosphate-phosphoric acid 25 mM, pH = 5.75 and the flow rate was 1.7 ml/min.…”