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PubMed1992

In a canine model, lung preservation at 10 degrees C is superior to that at 4 degrees C. A comparison of two preservation temperatures on lung function and on adenosine triphosphate level measured by phosphorus 31-nuclear magnetic resonance.

Techniques for organ preservation generally use hypothermia to retard metabolic requirements. However, excessive hypothermia may also produce injury. Using a canine left lung allotransplantation procedure, we compared two preservation temperatures (4 degrees and 10 degrees C) in terms of subsequent lung function measured by temporary occlusion of the right pulmonary artery after implantation of the preserved left donor lung. The lungs were flushed with low-potassium dextran electrolyte solution, inflated with 100% oxygen, and preserved for 18 hours. To investigate possible changes of energy stores at different temperatures, we performed phosphorus 31-nuclear magnetic resonance analyses of lung samples. Sequential determinations of adenosine triphosphate levels in lung tissue preserved at 4 degrees, 10 degrees, and 22 degrees C were studied. After transplantation, lungs preserved at 10 degrees C (n = 6) provided significantly better arterial oxygen tension than those preserved at 4 degrees C (n = 6), 451 +/- 46 mm Hg versus 243 +/- 86 mm Hg (p less than 0.05), and lower pulmonary vascular resistance, 581 +/- 68 dynes.sec.cm-5 versus 1006 +/- 157 dynes.sec.cm-5 (p less than 0.05). Adenosine triphosphate levels at 4 degrees and 10 degrees C were stable and did not differ from each other at the end of the 18-hour preservation period: 0.86 +/- 0.04 mumol/gm wet weight for control versus 0.86 +/- 0.07 mumol/gm wet weight for 4 degrees C and 0.93 +/- 0.06 mumol/gm wet weight for 10 degrees C after 18 hours of preservation. Preservation at 22 degrees C caused a 28% depression of adenosine triphosphate after 18 hours of preservation. These results lead us to conclude the following: (1) Optimal temperature for lung preservation is in the vicinity of 10 degrees C, and (2) lung dysfunction caused by excessive hypothermia is not due to a failure to maintain adenosine triphosphate levels. We suspect that adenosine triphosphate is generated by oxidative phosphorylation during lung preservation.

Adenosine Triphosphate↗

PubMed2006

Detection of significant stenotic lesions in the left anterior descending coronary artery using adenosine triphosphate stress strain imaging: comparison with coronary flow velocity reserve measurement using transthoracic Doppler echocardiography.

To evaluate the usefulness of adenosine triphosphate stress strain imaging for detecting significant coronary artery disease in the left anterior descending coronary artery (LAD), 34 patients underwent coronary flow velocity reserve measurement in the distal LAD and adenosine triphosphate stress strain imaging simultaneously. Time to peak strain (TPS) was measured in the apical septal segment. TPS ratio was obtained as the ratio between TPS at adenosine triphosphate stress and at baseline. TPS ratio in 11 patients with LAD lesions was significantly greater than that in 23 patients without LAD lesions (1.24 +/- 0.17 vs 0.92 +/- 0.12, respectively, P < .0001). With a cut-off value greater than or equal to 1.1 for the TPS ratio and less than 2.0 for the coronary flow velocity reserve, diagnostic accuracy for the presence of significant LAD lesions were 88% and 82%, respectively. In conclusion, strain imaging can differentiate ischemic and nonischemic myocardium accurately comparable with coronary flow velocity reserve measurement.

Adenosine Triphosphate↗

PubMedDate not supplied

Myocardial perfusion imaging with adenosine triphosphate predicts the rate of cardiovascular events.

BACKGROUND: Adenosine triphosphate (ATP) has effects similar to adenosine, including a very short half-life, with the advantage of a much lower cost. Our aim was to evaluate whether myocardial single photon emission computed tomography (SPECT) with ATP can predict the rate of hard events. METHODS AND RESULTS: We studied 299 patients (188 men; mean age, 64 +/- 10 years) with known or suspected coronary disease with thallium 201 SPECT during ATP infusion and at rest. Perfusion defects were divided into the following: absent/mild reversible, moderate/severe reversible, and mixed/fixed. During a maximum follow-up of 87 months (mean, 32.7 +/- 20.3 months), the rate of cardiovascular events was studied. The prognostic value of different variables that can influence survival was calculated with the Cox proportional hazards model. The total number of cardiovascular events was 115 (43 hard events). The annual rate of hard events according to type of perfusion defect was 3.44% (95% confidence interval [CI], 2.12-5.26) for absent/mild reversible, 6.06% (95% CI, 2.23-13.20) for moderate/severe reversible, and 15.12% (95% CI, 8.64-24.55) for mixed/fixed. In the Cox model the variables that significantly predicted hard events were age greater than 55 years (P = .0293), diabetes (P = .0036), and severe perfusion defects (P = .0008). CONCLUSION: ATP can be used for pharmacologic stress testing. SPECT with ATP has a stronger correlation with the rate of hard events than clinical variables.

Adenosine↗

PubMed1989

Modulation of platelet function by extracellular adenosine triphosphate.

A potential physiologic role of extracellular adenosine triphosphate (ATP) on platelet function is proposed in this report. It is widely accepted that ATP competitively inhibits adenosine diphosphate (ADP)-induced platelet aggregation. Our observations of platelet aggregation with the agonists, collagen, epinephrine, and ADP in the presence of 180 mumol/L ATP could support this competitive nature of ATP. However, the disaggregation of maximally aggregated platelets induced by ATP, theophylline, or ATP plus theophylline indicates that additional mechanisms of ATP action may be present. Extracellular gamma-32P-ATP (7 pmol) labels surface-membrane proteins in intact platelets as demonstrated by several criteria. The reaction is Ca++-dependent. Stimulation by calcium occurs in the physiologic range of 1 to 5 mmol/L. Significant levels of phosphorylation occur within one minute with near maximal levels reached by five minutes. Platelet cyclic AMP (cAMP) levels were elevated in a dose-dependent fashion in cells incubated for four minutes with increasing amounts of extracellular ATP (18 to 540 nmol). The addition of ATP plus theophylline resulted in a synergistic stimulation of cAMP levels. ATP was not being hydrolyzed to adenosine by plasma nucleotidases, as demonstrated by the lack of effect of ten U of adenosine deaminase. The phosphorylation of surface proteins by extracellular ATP released from activated platelets may modulate platelet responsiveness to agonists at distances removed from the site of vascular injury. Phosphorylation may also play a role in signal transduction to regulate the levels of intracellular cAMP, which further inhibits platelet activation.

Adenosine Triphosphate↗

PubMed2004

Role of extracellular adenosine triphosphate in human skin.

BACKGROUND: The nucleotide adenosine triphosphate (ATP) has long been known to drive and participate in countless intracellular processes. Extracellular ATP and its metabolite adenosine have also been shown to exert a variety of effects on nearly every cell type in human skin. Knowledge of the sources and effects of extracellular ATP in human skin may help shape new therapies for skin injury, inflammation, and numerous other cutaneous disorders. OBJECTIVE: The objective of this review is to introduce the reader to current knowledge regarding the sources and effects of extracellular ATP in human skin and to outline areas in which further research is necessary to clarify the nature and mechanism of these effects. CONCLUSION: Extracellular ATP seems to play a direct role in triggering skin inflammatory, regenerative, and fibrotic responses to mechanical injury, an indirect role in melanocyte proliferation and apoptosis, and a complex role in Langerhans cell-directed adaptive immunity.

Adenosine Triphosphate↗

PubMed1964

METABOLIC REGULATION OF ADENOSINE TRIPHOSPHATE SULFURYLASE IN YEAST.

de Vito, Peter C. (Princeton University, Princeton, N.J.), and Jacques Dreyfuss. Metabolic regulation of adenosine triphosphate sulfurylase in yeast. J. Bacteriol. 88:1341-1348. 1964.-The metabolic regulation of adenosine triphosphate sulfurylase (ATP-sulfurylase) from baker's yeast was studied. The enzyme was strongly inhibited by low concentrations of adenosine-5'-phosphosulfate, 3'-phosphoadenosine-5'-phosphosulfate, and sulfide. Sulfide ion was a competitive inhibitor of ATP-sulfurylase. Cysteine, methionine, sulfite, and thiosulfate were not inhibitors of the enzyme. ATP-sulfurylase was repressed when yeast was grown in the presence of methionine, and derepressed when yeast was grown in the presence of cysteine. In contrast to these results, the enzyme sulfite reductase was repressed in cysteine-grown cells. Thus, the sulfate-reducing pathway in yeast appears to be regulated at its first step both by feedback inhibition (by sulfide) and by repression (by methionine). Other known controls in the cysteine biosynthetic pathway are discussed.

Adenosine Triphosphate↗

PubMed1970

Adenosine triphosphate pools in Methanobacterium.

Certain aspects of adenosine triphosphate (ATP) metabolism in the strict anaerobe Methanobacterium strain M.o.H. have been investigated. Results of growth yield studies suggest that ATP conservation is very inefficient (0.06 mole of ATP per mole of hydrogen) under the conditions used to grow the bacterium in a fermentor. Experiments designed to demonstrate net ATP formation in cell-free extracts were negative. In whole-cell studies, substances which decreased ATP pool levels and increased adenosine monophosphate (AMP) pool levels were air, chloroform, 2,4-dinitrophenol, carbonylcyanide-m-chlorophenylhydrazone, and pentachlorophenol. The results suggest that the latter compounds act either as inhibitors of electron transport or as uncouplers of an energy-linked process. All the above compounds also inhibit methane formation in cell-free extracts, an ATP-requiring process. Methods are described for estimation of ATP, adenosine diphosphate (ADP), and AMP in whole cells, with a sensitivity in the range of 10 to 200 pmoles. An apparatus for quick sampling from an anaerobic suspension of whole cells also is described.

Adenine Nucleotides↗

PubMedDate not supplied

[From energetics to neurotransmission: adenosine triphosphate and its receptors].

INTRODUCTION AND AIMS: Adenosine triphosphate (ATP) is a substance that has stood out for being an energy donor, but today we know that it also has other functions. By activating a large variety of receptors that are widely distributed throughout the nervous system, ATP plays a role in neurotransmission, neuromodulation, apoptosis, cell proliferation and differentiation, pain, and so forth. AIMS: The aim of this study is to carry out a review of ATP receptors, their contribution to the correct functioning of neuronal circuits, and their involvement in the development of certain diseases. DEVELOPMENT: The issue is approached from different perspectives, such as the structure of ATP, its metabolism through ecto-ATPases and their main metabolite, adenosine, in addition to a detailed description of each of the purinergic receptors whose existence has been internationally accepted. We also examine how ATP and its receptors are involved in the structures of the nervous system, and more especially those that correspond to the sensory systems. CONCLUSIONS: The fact that purinoceptors are so widely distributed makes them worthy of a detailed examination. This new family of receptors promises to be a new diagnostic and therapeutic tool that enables us to approach certain aspects of the neurosciences from a new angle, by taking into account a new protagonist, ATP, in the generation of events that upset health.

Adenosine↗

PubMed1986

Intracellular compartmentalization of adenosine triphosphate.

The intracellular distribution and diffusivity of adenosine triphosphate (ATP) was studied by cryomicrodissection of individual Rana pipiens oocytes. We measured ATP concentrations in the nucleus, in animal and vegetal hemisphere cytoplasm, and in an intracellular reference phase (iRP, a microinjected gelatin "organelle") which samples diffusive ATP. Regional concentrations were not equal: nucleus much greater than animal ooplasm greater than vegetal ooplasm. ATP binding and water availability (as solvent) were determined by plotting nuclear and cytoplasmic ATP concentrations as a function of reference phase ATP concentrations (isothermal analysis). The nucleus/iRP isotherm for ATP was an equimolar line, showing that nucleoplasm resembles iRP gelatin (and consequently a simple aqueous solution) in its solvent properties. Cytoplasm/iRP isotherms were more complex, having slopes much less than unity and ordinal intercepts above the graph's origin. They demonstrate the presence in cytoplasm of mechanisms that are capable of excluding and binding ATP. These mechanisms are responsible for the inhomogeneity in ATPs intracellular distribution. In addition, exclusion and binding have different and opposing effects on ATP concentrations in the cell's "soluble space," and hence on ATP availability to enter into cellular reactions. It follows that these phenomena must be considered in attempts to model ATPs role in metabolism.

Adenosine Triphosphate↗

PubMed1994

[Adenosine triphosphate and supraventricular tachycardia].

UNLABELLED: Intravenously administered adenosine triphosphate (ATP) converts some supraventricular tachycardias to a sinus rhythm. Temporary atrioventricular block can help with the differentiation of different forms of supraventricular tachycardia. METHOD: Twenty-one patients with different forms of supraventricular tachycardia were subjected to electrophysiological examination for diagnostic or therapeutic (ablation) purposes. During tachycardia (after 5 minutes duration) ATP Spofa was administered by the i.v. route within 3 s into the cubital vein--0.3 mg per 1 kg body weight. RESULTS: One patient had two forms of supraventricular tachycardia. In the first group with auricular fibrillation (AF, n = 10), with auricular flutter (AFL, n = 5) and with automatic auricular tachycardia (AAT, n = 1) tachycardia was not eliminated by intravenously administered ATP. In the second group the authors were always able to eliminate paroxysmal supraventricular tachycardia, AV nodal reciprocal (AVNRT, n = 4) and atrioventricular reciprocal tachycardia (AVRT, n = 2) by intravenously administered ATP. CONCLUSIONS: 1. The authors conclude that ATP exerts an antiarrhythmic effect by blocking the reentry circuit in the AV node, i.e. it converts reentry supraventricular tachycardias (AVNRT and AVRT) to a sinus rhythm after reciprocal atrial activity. 2. The effect on atria can be proarythmogenic. 3. The authors did not confirm the effect on abnormal automaticity.

Adenosine Triphosphate↗

PubMed1991

[Vascular effects of adenosine-triphosphate].

This study assessed the effects of adenosine triphosphate (ATP) on systemic vascular resistances during the hypothermic cardiopulmonary bypass phase of cardiac surgery. Twenty patients scheduled for cardiac surgery were randomly divided into an ATP group (n = 10), and a placebo group (n = 10). Anaesthesia was similar for all the patients (diazepam, fentanyl and pancuronium). During the heart arrest phase, and as soon as the arterial pressure, the level in the venous return reservoir, and the pump flow rate had all been in steady state for 5 min, ATP or placebo was injected into the venous line of the oxygenator. Injection speed was doubled every three minutes, twice. The following ATP doses were administered: 0.012, 0.025 and 0.05 mg.kg-1.min-1. The level in the venous return reservoir was kept constant. Mean arterial pressure (MAP) and pump flow rate (DP) were assessed every half minute. Systemic vascular resistances were calculated with the relationship MAP/DP. Changes in vascular capacitance were directly proportional to changes in DP as the heart had been excluded, and all the blood returned to the pump, the blood volume being kept constant. MAP and DP remained unchanged in the placebo group. In the opposite ATP induced a dose-related systemic vasodilation: MAP decreased from 82.8 +/- 12.5 mmHg (control) to 66.0 +/- 14.8 mmHg, 59.8 +/- 10.6 mmHg, and 49.0 +/- 4.7 mmHg with 0.012, 0.025 and 0.05 mg.kg-1.min-1 ATP respectively. The MAP returned to preinfusion control levels when the ATP infusion was discontinued (90.0 +/- 17.8 mmHg). The DP, and therefore venous return, did not change, neither during ATP infusion, nor after its discontinuation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMedDate not supplied

Adenosine triphosphate (ATP) in human spermatozoa.

The seminal adenosine triphosphate (ATP) content was determined by bioluminescence after treatment with trichloroacetic acid (TCA) in 81 semen samples 1.5 h after ejaculation obtained from men attending our fertility clinic, and selected to contain either 20% or less spermatozoa with good progressive motility (n = 22), or 60% or more spermatozoa with good progressive motility (n = 59) (Study I), and in 18 semen samples from fertile men 30 min and 3.5 h after ejaculation (Study II). The latter samples were divided into 2 equally large groups according to sperm motility. In Study I the mean sperm ATP concentration was significantly higher in the semen samples with bad motility (0.63 nmol per living spermatozoa x 10(-6)) than in semen samples with good motility (0.39 nmol per living spermatozoa x 10(-6); P less than 0.01). In Study II the ATP concentration per living spermatozoa was also lower in the group with the best motility in comparison with the spermatozoa with lower motility (P less than 0.01), both 30 min and 3.5 h after ejaculation. During the 3-5 h incubation the sperm ATP concentration decreased by 21% (P less than 0.01) in the former group of samples but remained unchanged in the latter group. The results indicate that, in semen samples with highly motile spermatozoa, the consumption of ATP is higher than in semen samples with impaired sperm motility. It is therefore essential that the time between ejaculation and ATP measurement is as short as possible to obtain comparable results. Repeated ATP measurements in combination with an analysis of the number of living spermatozoa, may provide further information on the fertilizing capacity of spermatozoa.

Adenosine Triphosphate↗

PubMed2000

Cold preservation injury in rat liver: effect of liposomally-entrapped adenosine triphosphate.

BACKGROUND/AIMS: Energy charge and capacity for adenosine triphosphate (ATP) synthesis have been demonstrated to play a major role in the maintenance of organ function after liver preservation for transplantation. The aim of this study was to evaluate whether a supply of liposomally-entrapped ATP during preservation could improve the energy state and metabolism of cold-stored rat liver. METHODS: In the first set of experiments, the uptake of ATP-containing liposomes and their effects on hepatic viability were determined in isolated perfused unstored rat liver. In the second set of experiments, rat livers were preserved for 18 h at 4 degrees C in UW solution in the presence of these liposomes, and effects on energy state, cell volume and metabolism were evaluated. In each part, data were compared with adequate control, unloaded liposome-treated, and free ATP-treated groups (n=6 in each group). RESULTS: In non-stored livers, ATP-containing liposomes were taken up by the liver; they did not alter hepatic viability and induced a decrease in energy substrate consumption (glucose and amino acids), and an improvement in intrahepatic ATP content (+23% vs. Control). Addition of liposomally-entrapped ATP during cold storage produced a significant attenuation of the decrease in hepatic ATP content (Lip ATP 2: 524+/-45 vs. Control 2: 364+/-106 nmol/g; p<0.05), and induced, during reperfusion, a decrease in proteolysis associated with an increase in cell volume compared with the other groups (Lip ATP 2: 633+/-63 vs. Control 2: 532+/-38, Unloaded Lip 2: 483+/-55 and Free ATP 2: 500+/-29 microl/g; p<0.01). CONCLUSIONS: These data indicate that liposomally-entrapped ATP represents an effective means to improve liver graft energy state and function. The decrease in protein degradation may be related to the modification of cell volume.

Adenosine Triphosphate↗

PubMed1971

Adenosine Triphosphate Content of Selenastrum capricornutum.

The adenosine triphosphate content of Selenastrum capricornutum was maintained within 1.4 to 3.4 mug of adenosine triphosphate/mg (dry weight) of living biomass at different growth stages in media of different phosphorus concentrations.

Journal Article↗

PubMedDate not supplied

Captopril improves recovery of adenosine triphosphate during reperfusion of the ischemic isolated rat heart; a 31-phosphorus-nuclear magnetic resonance study.

The effect of captopril on energy-rich phosphates and pH during normothermic ischemic arrest, hypothermic cardioplegic arrest and subsequent reperfusion was investigated in the isolated rat heart using 31P-nuclear magnetic resonance. The hearts remained in the probe during all perfusion procedures and captopril (80 ml.l-1) treatment was started directly after cannulation. After normothermic ischemic arrest (15 min), the ATP content of captopril-treated hearts was not significantly different from that of untreated hearts (53 +/- 9% and 52 +/- 8%, respectively). Accumulation of inorganic phosphate at the end of ischemia was significantly less in treated hearts, suggesting a higher end-ischemic nucleotide content in treated hearts. Hypothermic cardioplegic arrest (St. Thomas' Hospital solution, 4 degrees C) lasted for 3 h at 10 degrees C. Adenosine triphosphate in untreated hearts was significantly lower at the end of ischemia; 36 +/- 6% compared to 53 +/- 9% for untreated hearts. Adenosine triphosphate in untreated hearts recovered to 76 +/- 9% after normothermic ischemia and to 72 +/- 7% after hypothermic ischemia at the end of 30 min reperfusion. Captopril significantly improved adenosine triphosphate recovery in both treated groups; 89 +/- 4% after normothermic and 83 +/- 4% hypothermic ischemia. We conclude that captopril has a beneficial effect on recovery of adenosine triphosphate both after normothermic and after hypothermic ischemia.

Adenosine Triphosphate↗

PubMed1967

The incorporation of inorganic phosphate into adenosine triphosphate by reversal of the sodium pump.

1. Resealed ghosts were prepared containing much potassium, very little sodium, and adenosine triphosphate (ATP), adenosine diphosphate (ADP) and (32)P-labelled orthophosphate (P(i)) at concentrations such that the ratio [ATP]/([ADP].[P(i)]) was low. Iodoacetate, iodoacetamide or both were also present. The ghosts were incubated in high-sodium, potassium-free media with and without ouabain, or in high-potassium media, and the incorporation of (32)P into ATP and ADP in 15 min was measured.2. There was some incorporation of (32)P into the nucleotides whatever the medium, possibly because of the residual activity of glycolytic enzymes, but in every experiment there was extra incorporation when the ghosts were in a high-sodium, potassium-free medium. This extra incorporation was largely abolished by ouabain (5 experiments) and partly abolished by oligomycin (1 experiment).3. It seems that if conditions are such that the over-all reaction associated with transport ATPase activity leads to an increase in free energy, the transport system will run backwards at a measurable rate and ATP will be synthesized at the expense of energy derived from ionic concentration gradients.4. The nature of the transport system is discussed in the light of the findings of this paper and the four preceding papers.

Adenine Nucleotides↗

PubMed2001

Augmented stretch activated adenosine triphosphate release from bladder uroepithelial cells in patients with interstitial cystitis.

PURPOSE: Extracellular adenosine triphosphate (ATP) has been shown to mediate inflammation and nociception and, therefore, it may have a role in symptoms associated with interstitial cystitis. We theorized that the bladder uroepithelium releases ATP in response to stretch and, furthermore, this process is augmented in interstitial cystitis. MATERIALS AND METHODS: We quantitated ATP using the luciferin-luciferase assay. Urinary ATP levels were compared in 35 patients with interstitial cystitis and in 33 normal controls after pH correction. Cultured interstitial cystitis and normal urothelial cells from the bladder biopsies of 5 patients each were stretched with the Flexcell 2000 machine (Flexcell International Corp., McKeesport, Pennsylvania) and supernatant ATP concentrations were measured. RESULTS: Mean urinary ATP plus or minus standard error of mean was significantly higher in patients with interstitial cystitis than in controls (L value 985 +/- 161 versus 377 +/- 27, p = 0.0007). Supernatant ATP released by stretched interstitial cystitis cells was stretch intensity dependent when comparing 0%, 10% and 20% elongation, and was also significantly higher in stretched interstitial cystitis than in stretched normal cells. CONCLUSIONS: Adenosine triphosphate was significantly elevated in the urine of individuals with interstitial cystitis and the stretch activated release of ATP was augmented in interstitial cystitis urothelium. Increased extracellular ATP may have a role in mechanosensory transduction and to our knowledge it represents a novel hypothesis.

Adenosine Triphosphate↗

PubMed1978

The use of adenosine triphosphate with magnesium chloride in the treatment of post ischemic renal injury.

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.

Adenosine Triphosphate↗