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At least 199 records · Page 11Linked to original sources
PubMed1987

Autonomic modulation of aminophylline influence on the electrophysiological effects of adenosine and adenosine triphosphate in the canine heart.

The influence of aminophylline, a competitive antagonist of adenosine, on the chronotropic and dromotropic effects of adenosine and adenosine triphosphate was studied in pentobarbital anaesthetised dogs under various modifications of the autonomic nervous tone. Adenosine and adenosine triphosphate (3 mumol.kg-1 each) were rapidly (greater than or equal to 1 s) injected into the right atrium during both sinus rhythm and right atrial pacing (cycle length 300 ms) before and after infusion of aminophylline (5 mg.kg-1) (n = 21) as well as after increasing doses of aminophylline (n = 10). Some dogs underwent either muscarinic blockade with atropine (0.2 mg.kg-1) (n = 10), or beta adrenergic blockade with propranolol (1 mg.kg-1) (n = 10), or complete autonomic blockade with atropine and propranolol (n = 10). Aminophylline (5 mg.kg-1) antagonised the negative chronotropic and dromotropic effects of adenosine triphosphate and adenosine in dogs pretreated with atropine or atropine plus propranolol but did not affect them in autonomically intact dogs. In addition, the electrophysiological effects of adenosine were antagonised by only the highest doses of aminophylline in autonomically intact dogs and by aminophylline (5 mg X kg-1) in dogs pretreated with propranolol. It was concluded that (a) alteration of the electrophysiological effects of adenosine triphosphate and adenosine by aminophylline is appreciably influenced by the autonomic nervous tone and (b) autonomic blockade is required for the manifestation of the antagonism by aminophylline of the electrophysiological action of adenosine and adenosine triphosphate.

Adenosine↗
PubMed1994

Lanthanide ions for the first non-enzymatic formation of adenosine 3',5'-cyclic monophosphate from adenosine triphosphate under physiological conditions.

Adenosine 3',5'-cyclic monophosphate (cAMP) is formed from adenosine triphosphate at pH 8 and 50 degrees C by use of lanthanide ions. Pr3+ and La3+ are the most active. The cAMP formation is more efficient at higher pH, where the mixture is made homogeneous by the addition of beta-cyclodextrin. The potential functioning of lanthanide ions as the catalytic center of an artificial adenylate cyclase is indicated.

Adenosine Triphosphate↗
PubMed2002

[Diagnostic use of adenosine triphosphate in cardiac arrhythmias].

Adenosine triphosphate (ATP) has been used for more than 50 years as a major medication in our therapeutic arsenal for the termination of supraventricular tachycardia crises for which the mechanism is re-entry implicating the atrioventricular node. In the present article other applications of ATP as a diagnostic agent for several cardiac arrhythmias are described: differential diagnosis of narrow or wide QRS tachycardia, diagnosis of a latent accessory pathway (intermittent or hidden), diagnosis of intranodal duality, and non-invasive evaluation of the results of the ablation of the slow pathway, and finally non-invasive diagnosis of the tachycardia mechanism in patients with palpitations or tachycardia with an obscure mechanism.

Adenosine Triphosphate↗
PubMed1999

Assessment of flow mismatch with pharmacologic stress test on myocardial contrast echocardiography in a model of critical stenosis: adenosine triphosphate and dipyridamole.

Although adenosine triphosphate (ATP) is a favorable vasodilator because of its short-acting duration, the agent's effectiveness in facilitating the diagnosis of myocardial ischemia with myocardial contrast echocardiography (MCE) is not fully understood. The goal of this study was to examine the efficacy of intravenous ATP administration (0.15 to 0.30 mg/kg/min for 5 minutes) in diagnosing the flow mismatch with MCE. To achieve this, a critical stenosis was produced in the left circumflex artery in 10 anesthetized dogs. The peak intensity ratio of risk area to control area was reduced by ATP from 0.51 +/- 0.19 to 0.31 +/- 0.12 (P <.05). Systolic wall thickening of the risk area did not change significantly (32.8% +/- 9.8% to 27.5% +/- 12.8%). These changes did not differ from those obtained after dipyridamole. We conclude that MCE with intravenous ATP administration is as useful as the dipyridamole method for diagnosing critical coronary stenosis.

Adenosine Triphosphate↗
PubMed1989

Structure and function of human hemoglobin covalently labeled with periodate-oxidized adenosine triphosphate.

Periodate-oxidized adenosine triphosphate (o-ATP), a ribose ring-opened dialdehyde derivative of ATP, reacts specifically with human deoxyhemoglobin to give a single major covalently modified product after reduction with sodium borohydride. This product, designated di-ATP Hb, was isolated using ion-exchange chromatography and shown to have incorporated two molecules of o-ATP/tetramer. Peptide mapping and x-ray crystallography at 2.8-A resolution indicate that a covalent adduct is formed between the ligand and residues Lys-82 EF6 of each beta chain in the organic phosphate-binding site of the molecule. di-ATP Hb exhibits a significantly decreased oxygen affinity (P50 = 20.8 mm Hg versus 5.8 mm Hg control; 50 mM 2-[bis(2-hydroxyethyl)amino]-2-(hydroxymethyl)-propane-1,3-diol, pH 7.4, 0.1 M C, 20 degrees C). The subunit cooper-activity of di-ATP Hb is also reduced (nmax = 1.9 versus 2.7 control).

Adenosine Triphosphate↗
PubMed1970

Brain adenosine triphosphate: decreased concentration precedes convulsions.

The concentration of adenosine triphosphate in the brain decreased before the onset of generalized convulsions in unanesthetized rats subjected to acute hypoxia or treated with hydroxylamine or pentylenetetrazole (Metrazol). As the convulsive episode continued, adenosine triphosphate decreased further. Stimulation of adenosine triphosphate production forestalled its disappearance from the brain and delayed the development of seizure activity.

Adenosine Triphosphate↗
PubMed1983

Modification of the cardiac action potential by intracellular injection of adenosine triphosphate and related substances in guinea pig single ventricular cells.

Effects of varying the intracellular adenosine triphosphate level on both the action potential and the membrane current were studied in single ventricular cells isolated from the guinea pig heart, using collagenase. Intracellular injection of adenosine triphosphate elevated the plateau potential level and prolonged the action potential duration. Similar results were obtained by injecting adenosine diphosphate, adenosine monophosphate, or creatine phosphate, i.e., substances considered to increase the intracellular concentration of adenosine triphosphate. In contrast, the action potential was depressed by procedures which could reduce the intracellular adenosine triphosphate level, such as an injection of creatine, superfusion of glucose-free Tyrode's solution containing 5.4 mM cyanide ion, or an injection of adenosine monophosphate into the cyanide-superfused cell. When the membrane current was recorded under the voltage clamp, it was found that the injection of adenosine triphosphate increased the amplitude of the slow inward current, whereas the superfusion of cyanide ion did not significantly decrease the slow inward current, although the action potential became considerably shorter. It was also found that the adenosine monophosphate injection decreased the amplitude of the net outward membrane current at the plateau level and increased it at around -40 mV, and thus intensified the N-shape of the isochronal 0.3-second current-voltage curve. The cyanide ion superfusion produced the opposite effect; in response to depolarizing clamp pulses more positive to the plateau level, the membrane current increased significantly with cyanide ion, but increased only slightly with adenosine triphosphate. These results suggest that intracellular adenosine triphosphate modifies the membrane currents at the plateau potential range, thus altering the action potential duration.

Action Potentials↗
PubMed1987

Enhanced myocardial protection with high-energy phosphates in St. Thomas' Hospital cardioplegic solution. Synergism of adenosine triphosphate and creatine phosphate.

The potential for improving myocardial protection with the high-energy phosphates adenosine triphosphate and creatine phosphate was evaluated by adding them to the St. Thomas' Hospital cardioplegic solution in the isolated, working rat heart model of cardiopulmonary bypass and ischemic arrest. Dose-response studies with an adenosine triphosphate range of 0.05 to 10.0 mmol/L showed 0.1 mmol/L to be the optimal concentration for recovery of aortic flow and cardiac output after 40 minutes of normothermic (37 degrees C) ischemic arrest (from 24.1% +/- 4.4% and 35.9% +/- 4.1% in the unmodified cardioplegia group to 62.6% +/- 4.7% and 71.0% +/- 3.0%, respectively, p less than 0.001). Adenosine triphosphate at its optimal concentration (0.1 mmol/L) also reduced creatine kinase leakage by 39% (p less than 0.001). Postischemic arrhythmias were also significantly reduced, which obviated the need for electrical defibrillation and reduced the time to return of regular rhythm from 7.9 +/- 2.0 minutes in the control group to 3.5 +/- 0.4 minutes in the adenosine triphosphate group. Under more clinically relevant conditions of hypothermic ischemia (20 degrees C, 270 minutes) with multidose (every 30 minutes) cardioplegia, adenosine triphosphate addition improved postischemic recovery of aortic flow and cardiac output from control values of 26.8% +/- 8.4% and 35.4% +/- 6.3% to 58.0% +/- 4.7% and 64.4% +/- 3.7% (p less than 0.01), respectively, and creatine kinase leakage was significantly reduced. Parallel hypothermic ischemia studies (270 minutes, 20 degrees C) using the previously demonstrated optimal creatinine phosphate concentration (10.0 mmol/L) gave nearly identical improvements in recovery and enzyme leakage. The combination of the optimal concentrations of adenosine triphosphate and creatine phosphate resulted in even greater myocardial protection; aortic flow and cardiac output improved from their control values of 26.8% +/- 8.4% and 35.4% +/- 6.3% to 79.7% +/- 1.1 and 80.7% +/- 1.0% (p less than 0.001), respectively. In conclusion, both extracellular adenosine triphosphate and creatine phosphate alone markedly improve the cardioprotective properties of the St. Thomas' Hospital cardioplegic solution during prolonged hypothermic ischemic arrest, but together they act additively to provide even greater protection.

Adenosine Triphosphate↗
PubMed1977

Formations of electrochemical proton gradient and adenosine triphosphate in proteoliposomes containing purified adenosine triphosphatase and bacteriorhodopsin.

Proteoliposome vesicles containing both bacteriorhodopsin of Halobacterium halobium and H+-translocating ATPase [EC 3.6,1.3] of a thermophilic bacterium, PS3, (TF0-F1) were reconstituted by either the dialysis method or the sonication method. Generation of the electrochemical proton gradient (deltamuH+) in these vesicles was measured using 9-aminoacridine for estimation of the chemical (deltapH) component and 8-anilinonaphthalene sulfonate for the electrical (deltaphi) component). In illuminated bacteriorhodopsin-vesicles the deltamuH+ reached 180-190 mV when reconstituted by the dialysis method and 210-220 mV when reconstituted by the sonication method. Vesicles reconstituted from both TF0-F1 and bacteriorhodopsin by the dialysis method generated a deltapH+ of about 200 mV on addition of ATP, while vesicles prepared by the sonication method generated very little deltamuH+, if any. These vesicles generated similar deltamuH+ on illumination to that found in bacteriorhodopsin-vesicles. Using vesicles reconstituted from both TF0-F1 and bacteriorhodopsin by the dialysis method, light dependent ATP synthesis was measured in relation to deltamuH+ formation. It was necessary to generate a deltamuH+ of above 170 mV for demonstration of appreciable formation of ATP and the greater the deltamuH+, the faster the rate of ATP synthesis.

Adenosine Triphosphatases↗
PubMed1968

Some aspects of adenosine triphosphate synthesis from adenine and adenosine in human red blood cells.

1. The synthesis of ATP has been studied in human erythrocytes. Fresh cells showed no net synthesis of ATP when incubated with adenine or adenosine, although labelled adenine was incorporated into ATP in small amounts.2. Cold-stored cells (3-6 weeks old) became progressively depleted of adenine nucleotides but incubation with adenosine or adenine plus inosine restored the ATP concentration to normal within 4 hr. Incorporation of labelled adenine or adenosine into the ATP of incubated stored cells corresponded to net ATP synthesis by these cells.3. Synthesis of ATP from adenosine plus adenine together was 75% derived from adenine and only 25% from adenosine, indicating that nucleotide synthesis from adenine inhibits the simultaneous synthesis of nucleotide from adenosine.

Adenine↗
PubMed1986

Gonadotropin depression of adenosine triphosphate levels and interaction with adenosine in rat granulosa cells.

Cellular ATP levels were measured with the luceferin-luciferase enzyme method in incubated preovulatory granulosa cells in vitro from PMSG-treated immature rats. The ATP levels were depressed by both FSH and LH, FSH being the more effective. Adenosine enhanced the ATP levels about 3-fold, but the depressive effects of gonadotropins could not be overcome by the addition of adenosine. Uptake of adenosine in granulosa cells followed Michaelis-Menten kinetics, with a Km of 15.9 +/- 3.6 microM and a maximum velocity of 1.6 +/- 0.1 pmol/min X 10(5) cells. The half-time for uptake of adenosine was about 40 min. The maximal uptake of adenosine was lowered from 48 +/- 5 to 30 +/- 1 pmol/10(5) cells by FSH treatment of the cells. The basal secretions of cAMP and progesterone from the granulosa cells were slightly but significantly enhanced by adenosine alone. Adenosine markedly enhanced FSH-stimulated cAMP secretion, but not progesterone secretion. A nonmetabolizable adenosine analog, 2-chloro-adenosine, did not affect the ATP levels or the secretion of cAMP from granulosa cells. This study confirms previous observations that adenosine can increase ATP levels and amplify the response to gonadotropins in gonadal cells. A novel finding is that the levels of ATP in granulosa cells are markedly depressed by gonadotropins. It is speculated that this depression of ATP may be a factor in the metabolic control of granulosa cells.

Adenosine↗
PubMed1990

Exogenous adenine nucleotides replete endothelial cell adenosine triphosphate after oxidant injury by adenosine uptake.

We studied the ability of human umbilical vein endothelial cells to recover from oxidant-induced ATP depletion. When endothelial cell ATP levels were depressed to 0.93 +/- 0.14 pmol/micrograms protein (compared with 4.96 +/- 0.6 pmol/micrograms protein in control cells) by hydrogen peroxide generated with 25 mU/ml glucose-glucose oxidase over 45 minutes, ATP levels returned to 1.73 +/- 0.21 pmol/micrograms protein during a 3-hour recovery period after oxidant injury ceased. When 25 microM ATP, ADP, AMP, or adenosine was added to the recovery media, intracellular ATP was significantly (p less than 0.001) increased to greater than 4.4 pmol/micrograms cell protein for each metabolite. HPLC of supernatants from oxidant-injured endothelial cells incubated with ATP, ADP, and AMP demonstrated extracellular metabolism of the adenine nucleotides to adenosine. When adenosine transport was inhibited with dipyridamole and nitrobenzylthioinosine, recovery of intracellular ATP by exogenous ATP, ADP, AMP, and adenosine was significantly (p less than 0.001) inhibited. Such cells were intact, as demonstrated by lack of LDH release. When oxidant stress was prolonged to 90 minutes, ATP depletion was irreversible, regardless of exogenously supplied adenosine; such cells demonstrated loss of cell integrity as demonstrated by release of intracellular LDH. Our results demonstrated that exogenous adenine nucleotides enhance recovery of oxidant-induced ATP depletion through metabolism to adenosine and subsequent adenosine uptake. Prolonged oxidant injury resulted in irreversible ATP depletion and loss of cell integrity that was not altered by exogenously supplied adenosine.

Adenine Nucleotides↗
PubMed1991

Evaluation of the invasive potential of superficial bladder cancer by adenosine triphosphate measurement.

In order to predict the malignant potential of superficial bladder cancer, in 121 patients with this malignancy adenine nucleotide levels (adenosine triphosphate, adenosine diphosphate, and adenosine monophosphate) and energy charge in bladder cancer cells were determined. The nucleotides were analyzed according to the method of Bücher, and the energy charge was calculated by applying the formula of Atkinson. It was clearly pointed out that superficial bladder tumors, which became invasive and/or metastatic, had higher levels of adenylate compounds than those which became not. Our results show that a high correlation exists between adenine nucleotide content and tumor progression.

Adenosine Diphosphate↗
PubMed1991

Platelet volume, aggregation, and adenosine triphosphate release in cerebral thrombosis.

We compared whole blood platelet aggregation, adenosine triphosphate release, platelet count, platelet crit (percentage volume of platelets), and mean platelet volume during the acute, subacute, and chronic periods of cerebral thrombosis in 22 patients with value in 29 controls. During the acute and subacute periods, platelet aggregation, platelet count, platelet crit, and mean platelet volume were significantly less in the patients than in the controls (p less than 0.05-0.01) while the adenosine triphosphate release rate per volume of platelets was significantly greater (p less than 0.05). During the acute period, infarct size showed a significant positive correlation with platelet aggregation (r = 0.59, p less than 0.01) and adenosine triphosphate release rate (r = 0.70, p less than 0.001) but a negative correlation with platelet count (r = -0.44, p less than 0.05). Our results suggest that platelet aggregation is reduced during the acute period due to the consumption of platelets during thrombogenesis but that the remaining individual platelets are hyperactive. Platelet consumption during the acute period increases with infarct size. During the chronic period, platelet crit and mean platelet volume were significantly less in the patients than in the controls (p less than 0.01) while the adenosine triphosphate release rate was significantly greater (p less than 0.01), suggesting sustained platelet consumption and chronically enhanced secretion of individual platelets.

Adenosine Triphosphate↗
PubMed1990

Depletion of myocardial adenosine triphosphate during prolonged untreated ventricular fibrillation: effect on defibrillation success.

We studied left ventricular endomyocardial adenosine triphosphate levels in 13 large mongrel dogs before and during ventricular fibrillation induced cardiac arrest to assess whether myocardial adenosine triphosphate content could predict successful cardiopulmonary resuscitation. Endomyocardial biopsies were performed during sinus rhythm (control), after 15 min of ventricular fibrillation or 10 min of ventricular fibrillation and 5 min of open chest cardiopulmonary resuscitation, after 20 min of ventricular fibrillation and 10 min of open chest cardiopulmonary resuscitation and after 40 min ventricular fibrillation and 15-20 min open chest cardiopulmonary resuscitation. Myocardial adenosine triphosphate was measured utilizing a bioluminescence method adapted for use with endomyocardial biopsies and normalized to protein content. Left ventricular endomyocardial adenosine triphosphate content fell significantly over time from a control level of 8.88 +/- 0.9 micrograms/mg protein to 5.73 +/- 0.5 micrograms/mg protein at 15 min of cardiac arrest, to 3.4 +/- 0.4 micrograms/mg protein after 30 min of cardiac arrest and to 1.98 +/- 0.3 micrograms/mg protein after 60 min of cardiac arrest (P less than 0.001). Adenosine triphosphate levels were significantly different between animals that received 10 min of ventricular fibrillation and successful open chest cardiopulmonary resuscitation and those that received 40 min of ventricular fibrillation and unsuccessful open chest cardiopulmonary resuscitation (4.35 +/- 0.48 vs. 2.11 +/- 0.43 micrograms/mg protein; P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗