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PubMed1998

[Detection of coronary artery disease by adenosine triphosphate stress echocardiography: comparison with adenosine triphosphate stress thallium myocardial scintigraphy and coronary angiography].

The clinical feasibility and usefulness of adenosine triphosphate-2Na (ATP) stress echocardiography for the detection of coronary artery disease (CAD) were assessed. Two-dimensional echocardiography and thallium-201 single photon emission computed tomography (SPECT) during ATP infusion were performed simultaneously in 58 consecutive patients (41 men and 17 women; mean age 66 +/- 12 years) with suspected CAD. ATP was infused intravenously at 0.16 mg/kg/min for 5 min and thallium was injected at 4 min. All patients underwent coronary angiography within 2 weeks of ATP echocardiography and ATP SPECT. An ischemic response during ATP infusion was detected by echocardiography as the development or worsening of a wall motion abnormality compared with the baseline and by SPECT as a perfusion defect that filled totally or partially during redistribution. Significant coronary artery stenosis was defined as > or = 75% diameter stenosis in a major epicardial vessel. The severity of the stenosis was classified as follows: Group A, lesions with significant coronary artery stenosis (> or = 75%, < 90%); Group B, lesions with severe coronary artery stenosis (> or = 90%) without collateral circulation; Group C, lesions with severe coronary artery stenosis (> or = 90%) with collateral circulation. Significant CAD was present in 43 of 58 patients. The overall sensitivity, specificity and accuracy of ATP echocardiography for detecting significant CAD were 70%, 100% and 78%, respectively, and those of ATP SPECT were 98%, 87% and 95%, respectively. In patients without previous myocardial infarction, the sensitivity of ATP echocardiography was 67%. The sensitivity of ATP echocardiography and ATP SPECT for detecting myocardial ischemia were 59% and 95% in patients with 1-vessel disease, 75% and 100% in those with 2-vessel disease, and 88% and 100% in those with 3-vessel disease, respectively. The induction of wall motion abnormality by ATP echocardiography was highly concordant with ATP SPECT imaging in patients with multivessel disease. Although the sensitivity of ATP echocardiography improved in patients with multivessel disease more than in those with single-vessel disease, detection of all diseased vessels was achieved in only 10% of patients with multivessel disease. The sensitivity of ATP echocardiography and ATP SPECT for detecting myocardial ischemia in individual vessels were: right coronary artery, 58% and 74%; left anterior descending artery, 59% and 97%; left circumflex artery, 27% and 68%. ATP-induced transient perfusion defects were associated with transient wall motion abnormality in only 57% of segments. The sensitivity of ATP echocardiography and ATP SPECT for detecting myocardial ischemia in patients with severe coronary stenosis were: Group A, 32% and 66%; Group B, 60% and 93%; Group C, 80% and 95%. The sensitivity of ATP echocardiography was significantly higher in the lesions with collateral circulation than in those without collateral circulation. ATP stress echocardiography is useful for detecting myocardial ischemia in patients with multivessel disease and in patients with severe coronary artery stenosis (> or = 90%). In particular, transient wall motion abnormality tends to be detected in the segments perfused by collateral circulation.

Adenosine Triphosphate↗
PubMed1993

Lysis of human monocytic leukemia cells by extracellular adenosine triphosphate: mechanism and characterization of the adenosine triphosphate receptor.

The present study shows that extracellular adenosine triphosphate (ATP) has the capacity to mediate dose-dependent lysis of the monocytic leukemia cell line THP-1. The lysis, assessed by 51Cr release, was found to be selective for ATP, because adenosine diphosphate (ADP) or other nucleotides were less effective in their ability to lyse the cells. The amount of 51Cr released was particularly enhanced by the stimulation of the cells with 1,000 U/mL of interferon gamma (IFN-gamma) for 3 days, and the sensitivity was time and dose dependent. Analysis of the mechanism of lysis indicated that the fully ionized form, ATP4-, mediated the lysis, because the addition of cation chelators or the absence of the divalent cations, Ca2+ and Mg2+, in the culture medium of a 6-hour 51Cr release assay increased the percent specific lysis. Therefore, the ATP receptors on THP-1 cells were classified as P2Z purinoceptors. Moreover, it is shown here that the Ca2+/calmodulin complex plays a role in the regulation of the lysis by extracellular ATP of THP-1 cells, because antagonists of this complex, such as trifluoperazine or KN-62, were found to inhibit the ATP-mediated cell lysis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2004

Human 3'-phosphoadenosine 5'-phosphosulfate synthetase (isoform 1, brain): kinetic properties of the adenosine triphosphate sulfurylase and adenosine 5'-phosphosulfate kinase domains.

Recombinant human 3'-phosphoadenosine 5'-phosphosulfate (PAPS) synthetase, isoform 1 (brain), was purified to near-homogeneity from an Escherichia coli expression system and kinetically characterized. The native enzyme, a dimer with each 71 kDa subunit containing an adenosine triphosphate (ATP) sulfurylase and an adenosine 5'-phosphosulfate (APS) kinase domain, catalyzes the overall formation of PAPS from ATP and inorganic sulfate. The protein is active as isolated, but activity is enhanced by treatment with dithiothreitol. APS kinase activity displayed the characteristic substrate inhibition by APS (K(I) of 47.9 microM at saturating MgATP). The maximum attainable activity of 0.12 micromol min(-1) (mg of protein)(-1) was observed at an APS concentration ([APS](opt)) of 15 microM. The theoretical K(m) for APS (at saturating MgATP) and the K(m) for MgATP (at [APS](opt)) were 4.2 microM and 0.14 mM, respectively. At likely cellular levels of MgATP (2.5 mM) and sulfate (0.4 mM), the overall endogenous rate of PAPS formation under optimum assay conditions was 0.09 micromol min(-1) (mg of protein)(-1). Upon addition of pure Penicillium chrysogenum APS kinase in excess, the overall rate increased to 0.47 micromol min(-1) (mg of protein)(-1). The kinetic constants of the ATP sulfurylase domain were as follows: V(max,f) = 0.77 micromol min(-1) (mg of protein)(-1), K(mA(MgATP)) = 0.15 mM, K(ia(MgATP)) = 1 mM, K(mB(sulfate)) = 0.16 mM, V(max,r) = 18.7 micromol min(-1) (mg of protein)(-1), K(mQ(APS)) = 4.8 microM, K(iq(APS)) = 18 nM, and K(mP(PPi)) = 34.6 microM. The (a) imbalance between ATP sulfurylase and APS kinase activities, (b) accumulation of APS in solution during the overall reaction, (c) rate acceleration provided by exogenous APS kinase, and (d) availability of both active sites to exogenous APS all argue against APS channeling. Molybdate, selenate, chromate ("chromium VI"), arsenate, tungstate, chlorate, and perchlorate bind to the ATP sulfurylase domain, with the first five serving as alternative substrates that promote the decomposition of ATP to AMP and PP(i). Selenate, chromate, and arsenate produce transient APX intermediates that are sufficiently long-lived to be captured and 3'-phosphorylated by APS kinase. (The putative PAPX products decompose to adenosine 3',5'-diphosphate and the original oxyanion.) Chlorate and perchlorate form dead-end E.MgATP.oxyanion complexes. Phenylalanine, reported to be an inhibitor of brain ATP sulfurylase, was without effect on PAPS synthetase isoform 1.

Adenosine Phosphosulfate↗
PubMed1997

Intracoronary administration of adenosine triphosphate increases myocardial adenosine levels and coronary blood flow in man.

Adenosine triphosphate (ATP) is reported to be released mainly from presynaptic vesicles and cardiomyocytes. The released ATP, which can be degraded to adenosine, may cause coronary vasodilation. However, there is no clear evidence that ATP is degraded to adenosine and causes coronary vasodilation in humans. The present study was undertaken to test whether intracoronary administration of ATP increases myocardial adenosine levels and coronary blood flow. In 11 patients, 3 doses of ATP (0.1, 0.2, and 0.4 mg) were injected into the left anterior descending coronary artery. The velocity of coronary blood flow was measured by Doppler flow probe, and the adenosine concentration in the coronary sinus blood was measured. We also continuously infused ATP (0.2 mg/min) for 1 min in another 10 patients. Coronary blood flow increased dose dependently soon after injection of ATP. Coronary arteriovenous differences in adenosine concentration increased [from 21 +/- 15 to 178 +/- 15 pmol/ml (p < 0.05) 10 sec after the injection of ATP (0.4 mg)] and there were marked reductions in both aortic blood pressure and heart rate. The adenosine levels returned to baseline 20 sec after the injection of ATP, and aortic blood pressure and heart rate also recovered, although coronary blood flow remained increased. Furthermore, continuous infusion of ATP for 1 min increased coronary blood flow velocity and coronary arteriovenous differences in adenosine concentration from 25 +/- 14 to 71 +/- 13 pmol/ml (p < 0.05) in 10 patients. These results indicate that intracoronary administration of ATP immediately increases coronary blood flow and the adenosine concentration of coronary venous blood, which returns to the baseline level thereafter. The differences in the time courses of increases in coronary venous adenosine levels and coronary blood flow after ATP injections suggest that vasodilatory mechanisms other than adenosine, eg, nitric oxide and prostaglandins, may also be involved in the ATP-induced coronary vasodilation. ATP may be used as a cardioprotective agent as well as adenosine.

Adenosine↗
PubMed1973

Quantitative extraction of adenosine triphosphate from cultivable and host-grown microbes: calculation of adenosine triphosphate pools.

EXISTING DATA ON ADENOSINE TRIPHOSPHATE (ATP) POOLS IN MICROBES ARE DEFICIENT FOR TWO REASONS: (i) incomplete extractions of ATP, and (ii) the failure to take into account that the adverse effects of extracting procedures on standard ATP exert analogous effects on the ATP released from bacterial cells. Methods for correcting observed yields and calculating ATP pools have been demonstrated. Three bacterial species were used in the studies on extraction of ATP: Escherichia coli, Mycobacterium phlei, and Mycobacterium lepraemurium. Perchloric acid and n-butanol were disqualified because of their failure to extract total bacterial ATP even from E. coli and because of inconvenient procedures. The new extraction procedure had minimal effects on standard ATP, liberated 100% of the ATP pools from the three representative species of microbes, and caused no ionic imbalance or quenching of bioluminescence. This method involves vortexing of cell suspensions for 10 s with 23% chloroform (vol/vol), heating at 98 C for the required time (E. coli, 3 min; M. phlei, 5 min; M. lepraemurium, 10 min) and then 1 min at 98 C with vacuum to dry the samples. Heat or chloroform alone may suffice for some microbes and release total ATP from plant and animal cells.

Adenosine Triphosphate↗
PubMed1996

Isoflurane preserves adenosine triphosphate levels in anoxic isolated rat hepatocytes by stimulating glycolytic adenosine triphosphate formation.

The hypothesis that general anesthetics protect energy reserves by decreasing energy demand is widely accepted but poorly substantiated. Isoflurane at clinical doses preserved adenosine triphosphate (ATP) levels in anoxic isolated hepatocytes. Specific inhibitors were used to block mitochondrial and/or glycolytic ATP formation to ascertain whether pathways of energy supply or demand, or both, were involved in ATP preservation by isoflurane. Hepatocytes were isolated from fed adult male rats after perfusing livers with Krebs buffer containing collagenase. Cells were incubated in Krebs buffer for 0-30 min at 25 degrees C under N2/CO2 (95%/5%) +/- isoflurane 0.63 mM in liquid phase. Oligomycin, iodoacetate, or fasting were used to block mitochondrial and glycolytic ATP formation. Under anoxia alone, ATP levels declined more slowly in the presence than in the absence of isoflurane, confirming the ATP-protective effect of isoflurane reported previously. With oligomycin plus iodoacetate blocking all ATP formation, ATP decline (representing pure ATP consumption) was not slowed by isoflurane. Isoflurane's protective effect recurred when glycolytic ATP supply was restored by incubating with oligomycin only. The protective effect was accompanied by increased lactate accumulation, and both effects-ATP preservation and lactate formation-were similarly dependent on isoflurane concentration. We conclude that the protective effect of isoflurane on energy status in anoxic isolated hepatocytes was not associated with reduced ATP demand but with enhanced ATP supply via stimulation of glycolysis.

Adenosine Triphosphate↗
PubMed1980

Hemolytic anemia in hepatic disease with decreased erythrocyte adenosine triphosphate.

Erythrocyte adenosine triphosphate (ATP) was assessed in patients with hepatic disease who had developed hemolytic anemia. Erythrocyte ATP was decreased, and this finding documents another cause for hemolytic anemia in patients with hepatic disease. The decreased erythrocyte ATP is secondary to hypophosphatemia, which is a common biochemical abnormality associated with hepatic disease.

Adenosine Triphosphate↗
PubMed1980

4-Aminopyridine blockade of neuronal depressant responses to adenosine triphosphate.

1 Adenosine, adenosine monophosphate and adenosine triphosphate (ATP) depressed the firing rate of neurones in the rat cerebral cortex when applied by microinontophoresis. 2 4-Aminopyridine, also applied iontophoretically blocked the depressant effects of the purines, without affecting responses to gamma-aminobutyric acid (GABA). This blockade was effected against purine depressions of both spontaneous and glutamate-evoked activity, suggesting that the interaction occurred postsynaptically.

4-Aminopyridine↗
PubMed1978

Antagonism by clonidine of neuronal depressant responses to adenosine, adenosine-5'-monophosphate and adenosine triphosphate.

1. Adenosine and its nucleotides adenosine-5'-monophosphate (AMP) and adenosine triphosphate (ATP) have been applied by microiontophoresis to neurones in the cerebral cortex of rats anesthetized with urethane. The firing rate of most neurones was depressed, though two cells were encountered which showed biphasic responses to ATP consisting of an initial excitation succeeded by depression. 2. The application of clonidine with iontophoretic currents of less than 25 nA resulted in blockade of the depressant responses to the purines, without affecting responses to noradrenaline, 5-hydroxytryptamine or gamma-aminobutyric acid (GABA). At much higher doses of clonidine, direct depression of cell firing occurred and occasional interaction with noradrenaline was noted. 3. In the case of the biphasic responses to ATP, clonidine seemed to block only the depressant phase. Reduction of the excitatory component paralleled changes of background firing. 4. It is concluded that, in common with some other 2-substituted imidazoline derivatives, clonidine possesses the ability to block responses to purine compounds.

Adenine Nucleotides↗
PubMed1996

The role of a purinergic P2z receptor in calcium-dependent cell killing of isolated rat hepatocytes by extracellular adenosine triphosphate.

Extracellular adenosine triphosphate (ATP o) (0.4 mmol/L), a P2-purinergic receptor agonist, induces cytolysis in several cell types including isolated rat hepatocytes. In this study, we investigated the P2-receptor involved in ATP o-induced, Ca2+-dependent cytotoxicity in hepatocytes. Pretreatment of hepatocytes with oxidized ATP, a P2z-receptor antagonist, or complexation of ATP(4-) (the agonist for the P2z-receptor) with an excess of Mg2+, prevented ATP o-induced cell death. Both protective treatments also prevented the development of a sustained high intracellular Ca2+ concentration as well as the subsequent accumulation of inorganic phosphate (Pi). The P2Z-receptor agonist 3'-O-'(4-benzoylbenzoyl)-ATP (BzATP) was twofold more potent than ATP in eliciting cytolysis, which was preceded by a sustained high intracellular Ca2+ concentration; pretreatment with oxidized ATP prevented both the increase in the intracellular Ca2+ concentration and cell death. Prevention of ATP o-induced cell death, as well as the increases in the intracellular Ca2+ concentration and inorganic phosphate (Pi) was also achieved by decreasing the pH o to 6.9. Together the findings indicate that Ca2+-dependent cell killing by extracellular ATP in hepatocytes is mediated by a P2Z-receptor. The cytolytic effects correlated specifically with a secondary "late" increase in the intracellular Ca2+ concentration.

Adenosine Triphosphate↗