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PubMed1986

Measurement of adenosine triphosphate and 2,3-diphosphoglycerate in stored blood with 31P nuclear magnetic resonance spectroscopy.

Conditions for blood storage are chosen to assure adequate levels of adenosine triphosphate (ATP) and 2,3-diphosphoglycerate (2,3-DPG). Because of the invasive nature of the techniques, biochemical assays are not routinely used to measure levels of these compounds in stored blood. However, 31P NMR spectroscopy measures phosphorylated intermediates in intact cells and could be used without disruption of the storage pack. We compared levels of ATP and 2,3-DPG measured by 31P spectroscopy and standard enzyme-linked biochemical assays in whole blood (WB) and packed red blood cells (PRBCs) at weekly intervals during a 35-day storage period. NMR demonstrated a marked decrease in 2,3-DPG and an increase in inorganic phosphate after the first week of storage. No significant differences in ATP concentrations were seen in WB during the storage period, but a significant decrease in ATP in PRBCs was documented. There was good agreement in levels of ATP and 2,3-DPG measured by NMR and biochemical techniques. 31P NMR spectroscopy is a noninvasive technique for measuring ATP and 2,3-DPG which has a potential use in quality assurance of stored blood.

2,3-Diphosphoglycerate↗
PubMed2000

Modulatory roles of the adenosine triphosphate P2x-purinoceptor in generation of the persistent nociception induced by subcutaneous bee venom injection in the conscious rat.

To study the role of adenosine triphosphate (ATP) P2x-purinoceptor in the persistent nociceptive response induced by subcutaneous (s.c.) bee venom injection, we used a selective P2x receptor antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), to evaluate whether spinal P2x receptor play a role in development of spontaneous persistent pain. Injection s.c. of bee venom into the plantar surface of one hindpaw in the conscious rat produces a monophasic, prolonged persistent nociception characterized by continuously flinching reflex of the injected paw for 1-2 h. Intrathecal (i.t.) pretreatment with PPADS at two lower doses of 5 and 10 microg resulted in suppression of the flinching reflex in a dose dependent manner with the inhibitory rate 37 and 44%, respectively, when compared with the control group; whereas i.t. PPADS at a higher dose of 30 microg failed to produce any inhibitory effect. This result suggests that activation of P2x-purinoceptor in the spinal cord contributes to the induction of bee venom-induced prolonged persistent pain. However, the antinociceptive effect of ATP P2x-purinoceptor antagonist such as PPADS on clinical pathological pain seems to be limited due to its lack of effectiveness at higher dose.

Adenosine Triphosphate↗
PubMed1988

Neutrophil-induced depletion of adenosine triphosphate in target cells: evidence for a hypochlorous acid-mediated process.

Human neutrophils, incubated with phorbol myristate acetate (PMA), caused a rapid and substantial adenosine triphosphate (ATP) depletion in lymphoblastoid Daudi cells without producing lysis. Catalase (which destroys hydrogen peroxide), taurine and methionine (which scavenge hypochlorous acid), and chloride omission from the medium prevented the ATP fall. An ATP depletion comparable to that induced by neutrophils was observed by replacing neutrophils with an appropriate myeloperoxidase-H2O2-Cl- enzymatic system. Together, these data suggest that the neutrophil ATP depleting activity involves the myeloperoxidase-catalyzed transformation of H2O2 into HOCl. Moreover, the free H2O2 remaining in the neutrophil extracellular environment is ineffective. In fact, a comparable amount of enzymatically generated H2O2 did not cause Daudi cell ATP loss. A direct role for H2O2 in the neutrophil-induced Daudi cell ATP depletion was observed only under artificial conditions, that is, in the presence of the heme enzyme inhibitor azide, which prevented the HOCl production but dramatically augmented the extracellular H2O2 level. Similar levels of ATP depletion in Daudi cells were induced by amounts of reagent HOCl comparable to those generated by neutrophils. As the generated HOCl can rapidly react with a variety of neutrophil-derived nitrogenous compounds (primarily ammonia and taurine) to yield chloramines, these chlorinated oxidants might contribute to the neutrophil-mediated ATP depletion. Nevertheless, the main and well-characterized chloramines (ammonia-derived monochloramine, NH2Cl, and taurine monochloramine, TauNHCl) were devoid of ATP-depleting capacity. Thus, the results suggest that the neutrophil-induced ATP depletion in Daudi cells is HOCl-dependent, is not mediated by NH2Cl or TauNHCl, and could be promoted either by HOCl directly or by an unknown derivative oxidant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

[Antiplatelet effect of adenosine triphosphate administration to animals under different experimental conditions].

A significant and considerable decrease in abnormally high platelet aggregation has been demonstrated after intramuscular administration of sodium adenosine triphosphate (ATP) to rats with depressed anti-coagulant system (in aging rats at the age of 11-12 months) and to rats with experimental diabetes both preliminarily and at the background of progressing diabetes. The elimination of one of thrombotic risk factors (decreasing elevated platelet aggregation) points to possible antithrombotic activity of ATP under these experimental conditions.

Adenosine Triphosphate↗
PubMed2002

Adenosine triphosphate accelerates recovery from hypoxic/hypoglycemic perturbation of guinea pig hippocampal neurotransmission via a P(2) receptor.

The present study was designed to assess the effects of adenosine triphosphate (ATP) on hippocampal neurotransmissions under the normal and hypoxic/hypoglycemic conditions. ATP reversely depressed population spikes (PSs), which were monitored in the dentate gyrus of guinea pig hippocampal slices, in a dose-dependent manner at concentrations ranged from 0.1 micro M to 1 mM. A similar depression was obtained with the P(2) receptor agonist, alpha,beta-methylene ATP (alpha,beta-MeATP), and the effect was inhibited by the P(2) receptor antagonists, suramin and PPADS. The inhibitory action of ATP or alpha,beta-MeATP was inhibited by the gamma-aminobutyric acid(A) (GABA(A)) receptor antagonist, bicuculline, but it was not affected by theophylline, a broad inhibitor of adenosine (P(1)) receptors, tetraethylammonium, a broad inhibitor of K(+) channels, or ecto-protein kinase inhibitors. ATP or alpha,beta-MeATP enhanced GABA release from guinea pig hippocampal slices, that was inhibited by deleting extracellular Ca(2+) or in the presence of tetrodotoxin, while ATP had no effect on GABA release from cultured rat hippocampal astrocytes or postsynaptic GABA-gated channel currents in cultured rat hippocampal neurons. Twenty-minutes deprivation of glucose and oxygen from extracellular solution abolished PSs, the amplitude recovering to about 30% of basal levels 50 min after returning to normal conditions. ATP or alpha,beta-MeATP accelerated the recovery after hypoxic/hypoglycemic insult (approximately 80% of basal levels). Adenosine diphosphate and adenosine monophosphate accelerated the recovery, but to a much lesser extent, and adenosine had no effect. The results of the present study thus suggest that ATP inhibits neuronal activity by enhancing neuronal GABA release via a P(2) receptor, perhaps a P2X receptor, thereby protecting against hypoxic/hypoglycemic perturbation of hippocampal neurotransmission.

Adenosine Triphosphate↗
PubMed1991

The effects of fructose on adenosine triphosphate depletion following mitochondrial dysfunction and lethal cell injury in isolated rat hepatocytes.

Mitochondrial injury in aerobic mammalian cells is associated with a rapid depletion of adenosine triphosphate (ATP) which occurs prior to the onset of lethal cell injury. In this report, the relationships between ATP depletion and lethal cell injury were examined in rat hepatocytes using oligomycin as a model mitochondrial toxicant and fructose as an alternative carbohydrate source for glycolysis. Oligomycin was more potent in causing lethal cell injury in hepatocytes isolated from fasted animals than cells from fed animals. The onset of cell injury (leakage of lactate dehydrogenase) in cells from fed animals correlated with the depletion of stored glycogen and ATP. The degree and time course profile of oligomycin-induced ATP depletion could be duplicated with 50 mM fructose alone in hepatocytes from fasted animals; however, fructose did not cause lethal cell injury. Oligomycin caused marked accumulation of adenosine monophosphate (AMP) and inorganic phosphate (Pi) and a conservation of adenine nucleotides. In contrast, fructose (50 mM) caused a decrease in Pi, no persistent change in AMP, and a depletion of the adenine nucleotide pool. Fructose, at concentrations greater than 1.0 mM, protected hepatocytes from oligomycin-induced toxicity. Blockade of mitochondrial ATP synthesis with oligomycin resulted in massive ATP depletion. In the presence of oligomycin, 5.0 mM fructose maintained cellular ATP content similar to that of control cells, whereas 50 mM fructose did not, demonstrating the biphasic effect of increasing fructose concentrations on cellular ATP content. Fructose-induced protection of hepatocytes from oligomycin toxicity was due to glycolytic fructose metabolism as hepatocytes incubated with iodoacetate (30 microM), fructose, and oligomycin had reduced viability and ATP content. In conclusion, interruption of mitochondrial ATP synthesis leads to marked ATP depletion and lethal cell injury. Cell injury is clearly not due to ATP depletion alone since increased glycolytic ATP production from either glycogen or fructose can maintain cell integrity in the absence of mitochondrial ATP synthesis and at low cellular ATP levels.

Adenosine Triphosphate↗
PubMed1967

The break-down of adenosine triphosphate in the contraction cycle of the frog sartorius muscle.

1. It is confirmed that a fluorodinitrobenzene (FDNB)-treated frog sartorius muscle does not split phosphorylcreatine in the course of its contraction cycle, but does use adenosine triphosphate (ATP).2. Good stoicheiometric relations between the diminution of ATP and the formation of adenosine diphosphate (ADP), adenosine monophosphate (AMP) and phosphate are obtained, and in a 0.2 sec tetanus at 0 degrees C the net break-down of ATP amounts to 0.27, the total equivalent break-down to 0.34 mumoles/g.3. There is no difference in this quantity between muscles interrupted at the height of contraction and those that have also relaxed, and, in experiments specifically designed to determine relaxation metabolism separately, no such metabolism is found. Thus, all the ATP-break-down occurs in the contraction phase.

Adenine Nucleotides↗
PubMed1994

[The clinical usefulness and efficacy of adenosine triphosphate in an emergency service].

We studied 89 patients diagnosed in our emergency department of paroxysmal supraventricular tachycardia, to describe the efficacy and safety of intravenous adenosine triphosphate (ATP) in their treatment. All received a first bolus of 10 mg of ATP and if no electrical response was observed, a second dose of 20 mg. This treatment was successful in 91% of the patients, lasting of 26.9 seconds to resolve the episode, and in the 53% of the patients with the first dose. In 9% of the patients ATP did not resolve the episode but allowed to diagnose it, which in five patients was atrial flutter, in 2 Wolff-Parkinson-White syndrome and in one atrial fibrillation. Adverse effects appeared in 25.6% of the cases, being in all transitory and banal. ATP is a very effective and safe drug for the treatment of patients with PSVT.

Adenosine Triphosphate↗
PubMed1984

Effect of adenosine triphosphate on the accessory pathways.

To determine the site of the anterograde and retrograde conduction in the Wolff-Parkinson-White syndrome (WPW), 40 mg of adenosine triphosphate (ATP) was injected during electrophysiological studies in 53 patients with ventricular preexcitation. In 40 cases, the accessory pathway was evident (group 1) and in 13 cases it was concealed (group 2). In 10 cases in group 1, anterograde conduction was abolished with disappearance of the features of preexcitation. In 7 patients of group 1 and in 4 patients of group 2, retrograde conduction in the accessory pathway was prolonged or abolished. These effects were unexpected because ATP is a parasympathomimetic drug. There was a correlation between the Kent effective refractory period (ERP) and the action of ATP. When the drug did not change the anterograde and retrograde conduction in the Kent bundle, the anterograde accessory pathway ERP was always less than 230 ms. When ATP only decreased retrograde conduction in the Kent bundle, anterograde accessory pathway ERP was always more than 280 ms.

Adenosine Triphosphate↗
PubMed1975

Demonstration of adenosine triphosphate hydrolysis in the enamel organ of the mouse incisor.

The hydrolysis of adenosine triphosphate in the mandibular enamel organ demonstrated that the Mg++-activated ATPase was destroyed by pre-treatment with either heat or alcohol, substrate specific for ATP, stimulated by the addition of glutathione or dinitrophenol, and inhibited by oligomycin. The distribution of reaction product was the same with Mg++, Mn++ or Zn++ as the activating cation. Omission of Mg++ from the incubation medium, or replacement with Ca++ or Sr++ resulted in marked hydrolysis of ATP in the cells associated with enamel matrix formation, with loss of enzyme activity in the cells of the zone of enamel matrix maturation. Hydrolysis of ATP by the cells of the stratum intermedium, stellate reticulum and papillary layer was dependent upon Mg++, Mn++, or Zn++.

Adenosine Triphosphatases↗
PubMed1988

Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node.

A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 +/- 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 +/- 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p less than 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 +/- 0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p less than 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.

Adenosine Triphosphate↗
PubMed2003

Glutathione and adenosine triphosphate content of in vivo and in vitro matured porcine oocytes.

Glutathione (GSH) content in mature porcine oocytes is correlated with subsequent fertilization and developmental success. Adenosine triphosphate (ATP) is an important energy source for maintaining cellular activities and protein synthesis. The objective of this study was to compare GSH and ATP concentrations of in vivo and in vitro matured porcine oocytes. Ovulated, in vivo matured oocytes were frozen at -80 degrees C in groups of 10-20 (GSH) or 5-10 (ATP). In vitro oocytes were matured in either tissue culture medium-199 (TCM199) supplemented with polyvinyl alcohol (PVA) or hyaluronic acid (MAP5), or North Carolina State University-23 (NCSU23) supplemented with porcine follicular fluid (pFF) and frozen as described, or fertilized and cultured. GSH content was determined by the dithionitrobenzoic acid-glutathione disulfide (DTNB-GSSG) reductase recycling assay. ATP content was determined by using the Bioluminescent Somatic Cell Assay Kit. Oocytes matured in vitro in defined TCM199 with PVA or hyaluronic acid, or NCSU23 with pFF had significantly lower concentrations (P < 0.05) of GSH (n = 207, 9.82 +/- 0.71 pmol/oocyte; n = 104, 9.73 +/- 0.81 pmol/oocyte; n = 108, 7.89 +/- 0.66 pmol/oocyte, respectively) compared to in vivo matured oocytes (n = 217, 36.26 +/- 11.00 pmol/oocyte). Concentrations of ATP were not different between treatments (in vivo, n = 70, 0.97 +/- 0.07 pmol/oocyte; TCM-PVA, n = 117, 0.81 +/- 0.13 pmol/oocyte; TCM-MAP, n = 107, 1.02 +/- 0.18 pmol/oocyte; NCSU-pFF, n = 134, 0.71 +/- 0.08 pmol/oocyte). Intracellular ATP content does not appear to be related to developmental potential in porcine oocytes. Low intracellular GSH may be responsible, in part, for lower developmental competence observed in in vitro matured porcine oocytes.

Adenosine Triphosphate↗
PubMed1991

[Thallium-201 myocardial scintigraphy after intravenous infusion of adenosine triphosphate disodium: a preliminary study in the diagnosis of coronary artery disease].

The feasibility and safety of thallium-201 myocardial scintigraphy after the intravenous infusion of adenosine triphosphate disodium (ATP) (Adetphos, Kowa) were studied in eight patients with angina pectoris and/or old myocardial infarction. Coronary arteriography (CAG) was performed by the conventional method in all patients. ATP was infused for 5 min and thallium was injected at 3 min after the start of ATP infusion. ATP was given at 0.12 mg/min/kg in two patients (group A), 0.16 mg/min/kg in three patients (group B), 0.20 mg/min/kg in one patient (group C) and 0.28 mg/min/kg in two patients (group D). SPECT images were obtained at 10 min and 180 min after thallium injection. No significant hemodynamic changes were observed in group A and B. Severe hypotension was observed in group C and one member of group D. Chest pain was experienced by one patient in group A, two in group B, one in group C, and both of the two in group D. ST depression on the electrocardiogram (ECG) was documented in one patient each of groups B and C. In one group D patient, the study was discontinued because of complete atrioventricular block persistent for 5 beats. The correlation between thallium imaging and CAG was unclear in group A, reasonable in groups B and C, and obscure in group D because of side effects. None of the patients who developed side effects of ATP were administered sublingual nitroglycerin or intravenous aminophylline. Their symptoms or ECG changes improved spontaneously within 2 min and disappeared within 5 min after termination of infusion. In conclusion, the optimal ATP regimen for this purpose was considered to be a 5 min infusion at 0.16 mg/kg/min and this method was found to be feasible and safe.

Adenosine Triphosphate↗
PubMed1997

Acidic conditions ameliorate both adenosine triphosphate depletion and the development of hyperpermeability in cultured Caco-2BBe enterocytic monolayers subjected to metabolic inhibition.

BACKGROUND: We recently reported that moderate degrees of adenosine triphosphate (ATP) depletion induced by chronic glycolytic inhibition or hypoxia increase the permeability of Caco-2BBe enterocytic monolayers. Interestingly, the development of lactic acidosis induced by anaerobic glycolysis ameliorates the development of hyperpermeability caused by chronic ATP depletion. We sought to further elucidate the mechanism(s) responsible for the apparent protection against epithelial hyperpermeability afforded by mild acidosis under conditions of metabolic inhibition. METHODS: Caco-2BBe monolayers growing on permeable supports in bicameral chambers were incubated with 2-deoxyglucose (2DOG) in a glucose-free (Glu-) environment to inhibit glycolysis. Permeability was determined by measuring the transepithelial flux of fluorescein sulfonic acid. Concentrations of intracellular calcium [Ca2+]i were determined fluorometrically by using fura-2. RESULTS: When extracellular pH (pH0) was maintained at 7.4 or 5.5, incubation of monolayers for 24 hours with Glu-/2DOG increased permeability and depleted intracellular ATP levels. However, keeping pH0 at 7.0 to 6.0 ameliorated both the development of hyperpermeability and the depletion of ATP induced by Glu-/2DOG. These protective effects were observed under acidic conditions created either by addition to the medium of HCl or by incubation under an atmosphere containing 20% CO2. Incubation with Glu-/2DOG caused bulging of the apical membranes of cells (electron microscopy) and derangements in the perijunctional distribution of actin (fluorescence microscopy); however, these structural changes were ameliorated by mild acidosis. Acute chemical hypoxia at pH0 7.4 induced by Glu-/2DOG plus antimycin A decreased cellular ATP levels and elevated [Ca2+]i. Lowering pH0 to 6.8 ameliorated both the depletion of ATP and the increase in [Ca2+]i induced by Glu-/2DOG+antimycin A. CONCLUSIONS: Moderate decreases in pH ameliorate the hyperpermeability induced by metabolic inhibition, possibly by diminishing ATP depletion and blunting increases in [Ca2+]i.

Acidosis↗
PubMed1996

[Transient atrioventricular conduction 1:1 in a patient with common atrial flutter following the administration of adenosine triphosphate].

A patient with atrial flutter and 2:1 atrioventricular conduction and acceleration to 1:1 conduction after administration of a single i.v. dose of 10 mg adenosin triphosphate (ATP) is presented. Despite the fact that ATP is a very useful drug for the treatment of paroxysmal supraventricular tachycardia. Its use as a diagnostic tool in atrial flutter must be carefully considered and the possibility of transient acceleration of AV conduction must be taken into account.

Adenosine Triphosphate↗
PubMed1995

Adenosine triphosphate stress echocardiography in the detection of myocardial ischemia.

The purpose of this study was to assess feasibility and safety in the diagnosis of coronary artery in the diagnosis of coronary artery disease and myocardial ischemia using adenosine triphosphate (ATP) stress echocardiography. ATP, a product of human myocardial tissue, is more potent than adenosine in increasing coronary blood flow. Like adenosine, ATP also has a short half-life (<10 s). Left ventricular echocardiograms were recorded during step-wise infusions of ATP in 86 patients who underwent coronary angiography and stress thallium 201 scintigraphy. No serious complications occurred with ATP infusion and most of the side effects were mild and transient. Significant coronary artery disease (>75% diameter stenosis) was present in 34 of 48 patients who had normal echocardiograms at rest. The sensitivity and specificity of ATP-induced wall motion abnormalities for coronary artery disease was 65% (22 of 34) and 100% (14 of 14), respectively. The sensitivity was 50% (10 of 20) in those with one-vessel disease and 86% (12 of 14) in those with multivessel disease (P < .05). In patients with normal echocardiograms at rest and without prior myocardial infarction, the sensitivity of ATP stress echocardiography for the detection of myocardial ischemia assessed by 201Tl single proton emission computed tomography was 58%, with a specificity of 76%, and a diagnostic accuracy of 66%. The sensitivity was 43% in those with one-vessel disease, and 86% in those with multivessel disease (P = .05). In patients with prior myocardial infarction, the sensitivity of ATP stress echocardiography for the detection of viable but jeopardized myocardium was 81%, with a specificity of 91%. The patients with well-developed collateral circulation had a higher incidence of developing wall motion abnormality than those without collaterals (70% v 40%, P < .01). ATP stress echocardiography is valuable for the assessment of coronary artery disease in patients with multivessel disease, coronary collaterals, and with prior myocardial infarction.

Adenosine Triphosphate↗
PubMed1994

P2Z adenosine triphosphate receptor activity in cultured human monocyte-derived macrophages.

The present study shows that human mononuclear phagocytes express a P2Z-like purinergic membrane receptor activity. Extracellular adenosine triphosphate (ATP) induces the formation of nonselective membrane pores in human mononuclear phagocytes that allow the entry of otherwise membrane impermeant fluorescent dyes (YO-PRO-1 or Lucifer yellow) into the cytoplasm of these cells. The percentage of mononuclear phagocytes that was permeabilized by ATP increased as monocytes matured into macrophages. Their response to ATP was inhibited by Mg2+ and oxidized ATP. Benzoylbenzoic-ATP (BzBzATP) was approximately 60% as effective as ATP and adenosine-5 -O-(thiophosphate) (ATP gamma S) was less than 20% as effective as ATP in permeabilizing human macrophages to YO-PRO-1 or Lucifer Yellow. Thus, the human P2Z-like receptor differs from its murine counterpart because BzBzATP, ATP, and ATP gamma S are equally efficacious in permeabilizing murine macrophage-like J774 cells to these dyes. UTP, GTP, and CTP were ineffective in permeabilizing human or murine macrophages to YO-PRO-1. Taken together, these data indicate that human monocyte-derived macrophages express a P2Z-like activity that is pharmacologically distinct from that expressed by their murine counterparts and that expression of these receptors is developmentally regulated in human mononuclear phagocytes.

Adenosine Triphosphate↗