Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT00586 (Adenosine triphosphate)
 903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Minipigs (20 to 25 kg.) were subjected to bilateral renal artery occlusion for 60 minutes. Renal blood flow was reduced to 65 per cent and glomerular filtration rate to 40 per cent of normal in control animals. Administration of adenosine triphosphate with magnesium chloride intravenously immediately after the period of ischemia resulted in restoration of renal blood flow to normal and glomerular filtration rate to 74 per cent of normal 24 hours later. Bilateral renal artery occulsion for 90 minutes resulted in a more severe impairment of renal function, which was not improved by the administration of adenosine triphosphate with magnesium chloride. Adenosine triphosphate with magnesium chloride may exert its effect by improving renal blood flow through inhibition of post-ischemic intrarenal vasoconstriction or possible by enhancing restoration of intracellular adenine nucleotides. The exact mechanism remains unclear.
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PMID:The use of adenosine triphosphate with magnesium chloride in the treatment of post ischemic renal injury. 75 14

The effects of high dose allopurinol (ALLOP) pretreatment on the cerebral energy metabolism of unanesthetized 7-day-postnatal rats during exposure to 3 h of cerebral hypoxia-ischemia were serially quantitated using non-invasive 31P NMR spectroscopy. Adenosine triphosphate, integrated over the last 2 h of hypoxia and expressed as a fraction of baseline, was 0.73 +/- 0.16 with ALLOP pretreatment (200 mg/kg s.c.) compared to 0.52 +/- 0.05 for saline pretreatment (P = 0.001). Inorganic phosphate/phosphocreatine (Pi/PCr), integrated over the same time interval, was 2.63 +/- 1.23 relative to baseline with ALLOP versus 5.13 +/- 1.45 for saline-treated pups (P less than 0.0005). We suggest that the neuroprotection achieved with high dose ALLOP pretreatment may be attributed in part to preservation of energy metabolites.
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PMID:Allopurinol preserves cerebral energy metabolism during perinatal hypoxia-ischemia: a 31P NMR study in unanesthetized immature rats. 143 87

Phosphorus 31 nuclear magnetic resonance spectroscopy was used to assess cerebral high-energy phosphate metabolism and intracellular pH in normoglycemic and hyperglycemic sheep during hypothermic circulatory arrest. Two groups of sheep (n = 8 per group) were placed in a 4.7-T magnet and cooled to 15 degrees C using cardiopulmonary bypass. Spectra were acquired before and during circulatory arrest and during reperfusion and rewarming. Intracellular pH and adenosine triphosphate levels decreased during circulatory arrest. Compared with the normoglycemic animals, the hyperglycemic group was significantly more acidotic with the greatest difference observed during the first 20 minutes of reperfusion (6.40 +/- 0.08 versus 6.08 +/- 0.06; p < 0.001). Intracellular pH returned to baseline after 30 minutes of reperfusion in the normoglycemic group but did not reach baseline until 1 hour of reperfusion in the hyperglycemic animals. Adenosine triphosphate levels were significantly higher in the hyperglycemic group during circulatory arrest. Repletion of adenosine triphosphate during reperfusion was similar for both groups. These results support the hypothesis that hyperglycemia during cerebral ischemia drives anaerobic glycolysis and thus leads to increased lactate production and an increase [corrected] in the intracellular acidosis normally associated with ischemia.
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PMID:Hyperglycemia increases cerebral intracellular acidosis during circulatory arrest. 144 97

The optimal level of hypothermia during myocardial preservation for cardiac transplantation is not known. Phosphorus 31 nuclear magnetic resonance spectroscopy was used to assess the effect of different preservation temperatures (15 degrees C in group 1, 4 degrees C in group 2) on the myocardial high-energy phosphate profiles during prolonged global ischemia and subsequent reperfusion of isolated rat hearts. Adenosine triphosphate depletion during ischemia was more gradual in group 2, leading to significant differences in myocardial adenosine triphosphate concentrations between the two groups after 3 hours of ischemia. The fall in intracellular pH during ischemia was significantly less pronounced in hearts preserved at 4 degrees C as compared with those at 15 degrees C. The postischemic recovery of both the left ventricular peak systolic pressure and the maximum rate of increase of left ventricular pressure was enhanced in group 2, although the ischemic period was 3 hours longer than in group 1. Hypothermia at 4 degrees C as compared with 15 degrees C appears to prolong myocardial protection with respect to adenosine triphosphate preservation, prevention of the fall in intracellular pH, and the enhancement of postischemic hemodynamic recovery.
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PMID:Optimal level of hypothermia for prolonged myocardial protection assessed by 31P nuclear magnetic resonance. 163 31

During both hemorrhagic shock and ischemia, adenosine triphosphate (ATP) concentrations fall in liver tissue. Incomplete recovery of ATP correlates with cell death and subsequent organ dysfunction. Changes in liver ATP levels were evaluated in paired groups of rats subjected to combined hemorrhagic shock and ischemia. A second set of paired animals was studied over time with shock alone. One animal in each pair was maintained at 28 degrees C and the other at 37 degrees C. Ischemia was produced by occluding inflow to the left half of the liver, and tissue was obtained from this area in all animals studied. Adenosine triphosphate levels fell in warm and cold animals subjected to both shock and 60 minutes of ischemia but recovered more completely during reperfusion in the cold animals. Shock alone caused a steady fall in ATP levels in the warm, but not the cold rats. These biochemical changes may indicate a beneficial effect of moderate hypothermia in the management of severe liver hemorrhage requiring temporary occlusion of blood flow.
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PMID:The effect of hypothermia on liver adenosine triphosphate (ATP) recovery following combined shock and ischemia. 174 Aug 1

Hyperkalaemia-induced hypopolarization of the sarcolemnal membrane during standard crystalloid cardioplegic arrest potentiates calcium influx during reperfusion and is associated with depletion of high-energy phosphate reserves. Adenosine has been shown to induce fast cardiac arrest whilst preserving membrane hyperpolarization in an isolated rat heart model. In this study we compared the efficacy of adenosine, both as an arresting agent and as an ultrastructural, haemodynamic and high-energy phosphate preserving agent, in an in situ global ischemia model in the baboon with St. Thomas' Hospital solution No. 2 (ST2; n = 8) and with Krebs-Henseleit buffer (KHB; n = 7). The addition of 10 mM adenosine to the non-cardioplegic KHB (ADO; n = 8) improved haemodynamic recovery significantly in terms of cardiac index (91.6% +/- 7.2 vs 59.9% +/- 9.9) and stroke volume index (101.6% +/- 8.9 vs 55.6 +/- 10.0) and was not statistically distinguishable from the ST2 with regard to cardiac index (91.6% +/- 7.2 vs 94.8% +/- 5.8), stroke volume index (101.6% +/- 8.9 vs 114.0% +/- 8.3) or left ventricular dP/dt (73.1% +/- 9.9 vs 87.0% +/- 12.4). Adenosine triphosphate was best preserved with ADO (103.5% +/- 21.1 vs 67.9% +/- 9.3 and 48.5% +/- 8.7) although this was not statistically significant. This suggests therefore that the mechanism of cardioprotection by adenosine occurs by means other than its role as high-energy phosphate precursor.
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PMID:Adenosine cardioplegia: reducing reperfusion injury of the ischaemic myocardium? 175 47

Interruption of hepatic blood supply for 60 min deteriorated liver mitochondrial respiratory functional indices--that is, respiratory control index (RCI) and the rate of oxygen consumption in state-III respiration (ST III O2). Recovery of ischemia-induced decreases in these functional indices in a saline-administered cirrhotic liver group was retarded compared with that in a normal liver group, and significantly low RCI and ST III O2 persisted 15 min after reperfusion. Prostaglandin E1 (PGE1) did not improve ischemia-induced decreases in RCI and ST III O2 but accelerated the recovery of mitochondrial respiratory function after reperfusion. Adenosine triphosphate (ATP) levels were markedly decreased during ischemia, and retardation of ATP recovery was also observed in rats with cirrhosis. PGE1 improved the recovery of ATP level in rats with cirrhosis. Liver blood flow in the cirrhotic liver was significantly lower than that of the normal liver. PGE1 enhanced liver blood flow. These results indicate that retardation of the recovery of RCI and ST III O2 in the cirrhotic liver might be based on the decrease in tissue blood flow and that agents increasing tissue blood flow might contribute to the acceleration of the recovery of mitochondrial respiratory function.
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PMID:Effects of prostaglandin E1 on the recovery of ischemia-induced liver mitochondrial dysfunction in rats with cirrhosis. 185 49

Ischemia/reperfusion injury to skeletal muscle may be explained by a cascade of cellular and systemic events initiated by an ischemic period followed by reperfusion. During the period of ischemia there is a gradual reduction of intracellular energy stores. Adenosine triphosphate is gradually depleted despite the buffering effect of creatine phosphate which is present in large stores in muscles. As well, glycogen stores are depleted with resultant production of small amounts of energy and large accumulations of lactate. Upon reperfusion there is a reactive hyperemia, resulting in an overall increase in muscle blood flow, despite the fact that areas may continue to be underperfused. Results of this blood flow are mixed with the beneficial effects of removing metabolic by-products and supplying exogenous substrates and oxygen. However, this blood flow also causes harmful effects by washing out necessary precursors for adenine nucleotide resynthesis. Production of oxygen free radicals occurs with resultant membrane lipid peroxidation, and calcium influx occurs upon reoxygenation with resultant disruption of oxidative rephosphorylation in the mitochondria. The sequestration of white blood cells in the muscle due to up regulation of both neutrophil receptors and endothelial leukocyte adhesion molecules results in a prolongation of the reperfusion injury. This subsequently results in damage to remote organs, including lung, heart, and kidneys. The future for therapeutic interventions aimed at reducing this injury lie mostly in the ability to modulate the reperfusion effect.
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PMID:Ischemia/reperfusion injury in skeletal muscle. 187 3

Repeated regional ischemia of short duration followed by reperfusion leads to preconditioning of the myocardium. Left anterior descending coronary artery (LAD) occlusion was applied for 5 minutes and then released for 10 minutes. This was repeated four times by using an intact pig model. LAD occlusion was then continuously applied for 1 hour. Myocardial function, high energy phosphates, and membrane phospholipids were compared with a control (nonstunned) group over a 6-hour reperfusion period. Stunning itself produced no significant change in regional function, total phospholipids, or free fatty acids (FFA). However, regional function, adenosine triphosphate, and creatine phosphate were significantly (p less than 0.05) reduced over control. After 60 minutes of ischemia, regional function was significantly improved by preconditioning that persisted throughout reperfusion (p less than 0.01). This was associated with an 11% mean decrease in infarct size (p less than 0.05). Adenosine triphosphate was significantly preserved during ischemia in the preconditioned hearts, and this preservation persisted throughout reperfusion (p less than 0.05). Total phospholipids were not affected by ischemia in either group. However, during reperfusion both groups demonstrated a 15-20% decrease in phospholipid levels at 1 hour, with only the stunned group showing a progressive increase at 3 and 6 hours (p less than 0.05). Examination of FFA during reperfusion demonstrated a profound increase in only the unstunned animals (p less than 0.05), correlating with the decreased level of membrane phospholipids noted in this group. In conclusion, repeated stunning predisposes the heart to recovery after regional ischemia. This results in improved mechanical function, increased high-energy phosphate stores, and decreased infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preconditioning the heart by repeated stunning improves myocardial salvage. 193 32

Hypothermic storage of cardiac allografts is routinely used for transplantation but is associated with an increased mortality when ischemic times are greater than 4 hours. The ideal storage conditions (solution and temperature) could extend the current limits of cold ischemia. Human endothelial cells and ventricular myocytes were studied to screen various solutions and temperatures for organ preservation. Four solutions (modified Euro-Collins, phosphate-buffered saline, Stanford cardioplegia, and University of Wisconsin) were evaluated. Endothelial cells were evaluated after prolonged hypothermic storage consisting of 0 degree, 4 degrees, and 8 degrees C for 36 hours, and ventricular myocytes were stored at 0 degree and 8 degrees C for 24 hours. Cell viability was determined by morphology (10 dishes per group), and trypan blue exclusion (5 dishes per group) in addition to a cell adhesion assay (endothelial cells 5 dishes per group) and adenine nucleotide analysis with high-performance liquid chromatography techniques (ventricular myocytes 5 dishes per group). Endothelial cell morphology was best preserved by University of Wisconsin solution (p less than 0.001, chi 2) and at 0 degree C (p less than 0.01, chi 2). Endothelial cells stored with University of Wisconsin solution excluded trypan blue better (1.0% +/- 0.5% cells stained, p less than 0.001. Analysis of variance [ANOVA]). Cell adhesion was poorly protected with Stanford cardioplegia (p less than 0.001, ANOVA). Myocyte morphology was preserved best with University of Wisconsin solution at 0 degree C (p less than 0.001, chi 2). According to trypan blue staining, Euro-Collins and University of Wisconsin solutions were superior to Stanford cardioplegia or phosphate-buffered solutions (p less than 0.001, ANOVA). Temperature did not influence the trypan blue results. Adenosine triphosphate was maintained best with University of Wisconsin solution at 0 degree C (p less than 0.01, ANOVA). Myocytes were more sensitive to the effects of prolonged storage compared with endothelial cells by morphologic criteria and trypan blue staining characteristics, irrespective of the shorter preservation times. University of Wisconsin solution was the most effective solution tested. Colder temperatures (0 degree to 4 degrees C) provided better protection than 8 degrees C. Myocytes were more sensitive to prolonged preservation than endothelial cells. Furthermore, the technique used appears helpful as a model of prolonged hypothermic storage and could be expanded to assess other interventions.
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PMID:Prolonged hypothermic cardiac storage with University of Wisconsin solution. An assessment with human cell cultures. 194 84


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