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PubMed1995

Extracellular adenosine triphosphate. A shock to hemopoietic cells.

Many or perhaps all cell types in the body possess extracellular binding sites for nucleosides and nucleotides, the purinoceptors. The binding sites that favor adenosine triphosphate (ATP) have been classified as P2-purinoceptors. One subclass of the P2-purinoceptors is the P2z-purinoceptor that mediates the permeabilizing effect of ATP4- (the fully ionized form of adenosine triphosphate). In the presence of millimolar concentrations of ATP4-, this receptor, which was found on all cells of hemopoietic origin but not on cells of stromal origin, renders the sensitive cells permeable for molecules up to 1 kD. This property has been used to eliminate cells of hemopoietic origin from mixed populations. Skeletal- and blood-forming tissues have a complex cellular composition of predominantly stromal and hemopoietic cells. The 2 cell types influence each others' formation, differentiation, and activities in a largely unclarified manner. Rigorous separation would help the study of the properties and potencies of the 2 cell types and their mutual interactions. A short treatment of cell populations isolated from bone, bone marrow, or cartilage with 2 mM adenosine triphosphate and 1 mM of cytotoxic, but not permeant, potassium thiocyanate obliterates all cells of hemopoietic origin, including macrophages, osteoclasts, and their progenitors from these populations.

Adenosine Triphosphate↗
PubMed1992

The effect of hypothermia on liver adenosine triphosphate (ATP) recovery following combined shock and ischemia.

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.

Adenosine Triphosphate↗
PubMed1998

Fructose-1,6-bisphosphate preserves adenosine triphosphate but not intracellular pH during hypoxia in respiring neonatal rat brain slices.

BACKGROUND: Fructose-1,6-bisphosphate (FBP) sometimes provides substantial cerebral protection during hypoxia or ischemia. 31P/1H nuclear magnetic resonance spectroscopy of cerebrocortical slices was used to study the effects of FBP on hypoxia-induced metabolic changes. In addition, 13C-labeled glucose was administered and 13C nuclear magnetic resonance spectroscopy was used to search for FBP-induced modulations in glycolysis and the pentose-phosphate pathway. METHODS: In each experiment, 80 slices (350 microm) obtained from ten 7-day-old Sprague-Dawley rat litter mates were placed together in a 20-mm nuclear magnetic resonance tube, perfused, and subjected to 30 min of hypoxia (PO2 < 3 mmHg). Nine experiments were performed, with n = 3 in each of three groups: (1) no treatment with FBP; (2) 60 min of prehypoxia treatment with FBP (2 mM); and (3) 60 min of posthypoxia treatment with FBP (2 mM). 31P/1H Interleaved nuclear magnetic resonance spectra at 4.7 T provided average adenosine triphosphate, intracellular pH, and lactate. Cresyl violet stains of random slices taken at predetermined time points were studied histologically. Some experiments had [2-13C]glucose in the perfusate. Slices from these studies were frozen for perchloric acid extraction of intracellular metabolites and studied with high-resolution 13C nuclear magnetic resonance spectroscopy at 11.75 T. RESULTS: With no pretreatment with FBP, hypoxia caused an approximately 50% loss of adenosine triphosphate, an approximately 700% increase in lactate, and a decrease in intracellular pH to approximately 6.4. Pretreatment with FBP resulted in no detectable loss of adenosine triphosphate, no increase in lactate, and minimal morphologic changes but did not alter decreases in intracellular pH. 13C Nuclear magnetic resonance spectra of extracted metabolites showed that pretreatment caused accumulation of [1-13C]fructose-6-phosphate, an early pentose-phosphate pathway metabolite. Posthypoxic treatment with FBP had no effects compared with no treatment. CONCLUSIONS: During severe hypoxia, pretreatment with FBP completely preserves adenosine triphosphate and almost completely preserves cell morphology but does not alter hypoxia-induced decreases in intracellular pH. Pretreatment also substantially augments the flux of glucose into the pentose-phosphate pathway.

Adenosine Triphosphate↗
PubMed1992

Cardioplegia with adenosine and adenosine triphosphate in the isolated guinea pig heart.

In order to determine the effect of adenosine triphosphate (ATP) and adenosine in cardioplegic solutions, a comparative study has been undertaken in isolated guinea pig hearts using the Langendorff perfusion technique as a model of cardiopulmonary bypass. The hearts (n = 10 in each group) previously being perfused by Krebs-Henseleit solution, were arrested by one of the following cardioplegic solutions: 1) Potassium 20 mM/L (Plegisol), 2) Potassium 20 mM/L+ATP 10 mM/L, 3) Adenosine 10 mM/L, 4) Adenosine 10 mM/L+ATP 10 mM/L. After 45 min of hypothermic ischemia, postischemic recovery of heart rate, ventricular contractility, heart work and postischemic changes in tissue enzymes (LDH, SGOT, SGPT) were compared among the 4 different cardioplegic solutions. Arrest time and number of arrest beats were also recorded and compared among the groups. Although similar beneficial results on postischemic recovery were achieved with adenosine cardioplegia and with ATP supplemented potassium cardioplegia, ATP supplemented adenosine cardioplegia did not show any beneficial effects on postischemic recovery.

Adenosine↗
PubMed1984

Cyclosporine-induced adenosine triphosphate depletion in murine T and B lymphocytes.

Adenosine metabolism in C57BL/6 mouse spleen cells was studied. Adenosine triphosphate (ATP) levels in resting T cells were 26.9 +/- 3.4 ng/10(5) cells compared with 16.5 +/- 3.1 ng/10(5) cells in resting B cells. Cyclosporine (CSA) caused a prompt and severe ATP depletion in both T and B cells, which could be mitigated by the addition of adenosine. B cell ATP levels were returned to normal while T cell levels were only partially restored. The adenosine deaminase inhibitor erythro-9-(2 hydroxy-3 nonyl) adenine (EHNA) also caused ATP depletion in T and B cells, which could similarly be prevented in part by the addition of adenosine. However, when CSA and EHNA were combined, adenosine could no longer protect ATP pools and severe ATP depletion in T and B cells occurred. This suggests that CSA and EHNA affect different steps in the conversion of adenosine to ATP. Although both T and B cell ATP levels were affected by CSA, the ability of supplementary substrate to restore ATP levels to normal in B cells but not in T cells may explain the apparent selective effect of CSA impairing T cell functions with sparing of B cell functions. Furthermore, if causing ATP depletion is associated with immunosuppressive activity, EHNA may be useful in potentiating the immunosuppressive effects of CSA.

Adenine↗
PubMed1997

Adenosine triphosphate and hemoglobin in vasospastic monkeys.

Adenosine triphosphate (ATP) is a vasoactive compound found in high levels inside erythrocytes that may contribute to vasospasm occurring after subarachnoid hemorrhage (SAH). This study was instituted to test whether ATP causes vasospasm in a monkey model. Thirty-two monkeys were randomized to four groups of eight monkeys each to undergo cerebral angiography at baseline (Day 0) and then at Day 7 after subarachnoid placement of: 1) agarose, 2) ATP in agarose, 3) autologous hemolysate in agarose, or 4) purified human hemoglobin A(0) in agarose. Vasospasm was assessed by comparison of Day 0 and Day 7 angiograms between and within groups and by pathological examination of a subset of perfusion-fixed monkeys. Levels of adenine nucleotides were measured on Day 7 in subarachnoid agarose by high-pressure liquid chromatography. There was significant vasospasm of the right middle cerebral artery in groups given ATP (-28 +/- 7% reduction, paired t-test, p < 0.05), hemolysate (-23 +/- 7%, p < 0.05), or pure hemoglobin (-15 +/- 2%, p < 0.005). Analysis of variance revealed no significant differences between groups in diameters of cerebral arteries on Day 7. Pathological examination showed mild inflammation in the subarachnoid spaces of animals exposed to hemolysate or hemoglobin and less inflammation in those given ATP or agarose. There were no pathological changes in the cerebral arteries of animals in any group. Most of the ATP diffused out of the subarachnoid agarose by Day 7, and levels of adenine nucleotides in subarachnoid agarose were higher on Day 7 in animals exposed to hemoglobin or hemolysate. It is concluded that ATP could contribute to vasospasm occurring after SAH but that further investigations are necessary to determine if levels of ATP adjacent to vasospastic arteries are sufficient to contribute to vasospasm. In addition, no observation was made of severe vasospasm with histopathological changes in the arteries equivalent to that produced by whole blood clot in the subarachnoid space of monkeys. It should be determined whether this is because a single compound, such as ATP or hemoglobin, causes vasospasm, but that placing the compound in agarose alters its delivery and decreases the amount of vasospasm produced, or whether vasospasm is a more complex, multifactorial process.

Journal Article↗
PubMed1965

Adenosine triphosphate pool during the growth cycle in Streptococcus faecalis.

Forrest, W. W. (University of Adelaide, Adelaide, South Australia). Adenosine triphosphate pool during the growth cycle in Streptococcus faecalis. J. Bacteriol. 90:1013-1018. 1965.-The adenosine triphosphate (ATP) pool has been studied throughout the growth cycle of Streptococcus faecalis. Normally, the pool is quantitatively related to the concentration of organisms and the growth rate, but deviations from these relationships can occur without affecting the growth rate of the organisms. A critical concentration of ATP seems necessary for exponential growth, and, at lower levels, only linear growth can occur. If no growth can take place, catabolism of added energy source gives rise to a large increase in the pool level. The pool level represents the balance between the demands of the organisms for energy and the supply of energy derived from catabolism of the substrate.

Adenosine Triphosphate↗
PubMed2002

[Effect of acrylamide on creatine kinase and adenosine triphosphate in brain of mice and its significance].

OBJECTIVE: To explore the changes of brain energy metabolism following acrylamide (ACR) poisoning. METHODS: Creatie kinase (CK), adenosine triphosphate (ATP), adenosine diphosphate(ADP), adenosine 5'-monophosphate(AMP) and glucose contents in brain were observed in O1a mice and 6J mice following ACR intoxication by enzyme analytical method. RESULTS: ATP, CK and glucose levels decreased transiently in O1a mice, while ATP level in 6J mice was significantly decreased (1.76 mumol/g, P < 0.01), as compared to the control (2.53 mumol/g) but ADP and AMP were increased, glucose was decreased. The activity of CK in poisoned group (1.13 mumol/g, P < 0.01) was lower than that of control (3.16 mumol/g and lasted for 5 weeks). CONCLUSION: The influence of ACR on O1a mice was slight and reversible but on 6J mice was severe and lasting. There was severe damage to the potential energy supply compensation, which might be the biochemical basis of neuron damage induced by acrylamide.

Acrylamide↗
PubMed1985

Adenosine triphosphate degradation in specific disease.

Two hypotheses concerning adenosine triphosphate (ATP) degradation are examined: The metabolic basis of specific disorders involves ATP degradation, and uric acid and its precursors are measurable body fluid markers of ATP degradation. These hypotheses are examined by discussing human models of ATP degradation, methods for measurement of ATP degradation, and disorders of ATP degradation.

Adenine↗
PubMed2000

Expression of inducible nitric oxide synthase mRNA and production of nitric oxide are induced by adenosine triphosphate in cultured rat microglia.

The effect of adenosine triphosphate (ATP) on the expression of the inducible nitric oxide synthase (iNOS) mRNA and production of nitric oxide in cultured rat microglia was examined. ATP induced iNOS mRNA dose-dependently (100-1,000 microM). The induction began within 1 h after addition of ATP (100 microM) with peak expression occurring at 6 h. The release of nitric oxide to culture medium was significantly increased by the treatment with ATP (100 and 1,000 microM) for 12 and 24 h. These results indicate that ATP is a potential mediator to induce iNOS mRNA expression and NO production in microglia.

Adenosine Triphosphate↗
PubMed1993

[Efficacy of adenosine triphosphate in terminating supraventricular tachycardia].

The efficacy of adenosine triphosphate (ATP) was tested in 23 patients suffering from supraventricular tachycardia; 10 patients had orthodromic circus movement tachycardia and 13 typical av nodal reentrant tachycardia. At a mean dose of 0.18 mg/kg all tachycardias were halted in less than 1 minute due to transient acute av nodal block followed by return to normal av conduction within 8 seconds. All patients had transient minor side effects. One elderly subject had a short episode of atrial fibrillation after the acute av block. In conclusion, ATP is useful and safe for rapid termination of supraventricular tachycardias incorporating the av node in their circuit.

Adenosine Triphosphate↗
PubMed1975

Radiation-induced decrease in influx rates of potassium ions into thymocytes in vitro in relation to decreased intracellular adenosine triphosphate concentrations.

The relationship between decreases in the adenosine triphosphate content of irradiated thymocytes and observed changes in the influx constant values for potassium ions in the same cells have been investigated. The results suggest that radiation-reduced ATP concentrations may be a rate-limiting factor controlling the active transport of potassium, 3--4 hours after X-irradiation in the range 2--20 krad. However, over the first hour of incubation, post-exposure ATP levels have not decreased sufficiently to be a major factor in the observed decrease in active uptake of potassium ions. This evidence is supported by comparisons of the influence of 1 mM adenine on radiation-reduced ATP levels and influx constants over the first hour after irradiation.

Adenosine Triphosphate↗
PubMed1966

Light induced concentration changes of adenosine-triphosphate in phycomyces sporangiophores.

The concentrations of extractable adenosine triphosphate (ATP) following the induction of positive light-growth responses in Phycomyces sporangiophores by blue light stimuli have been measured by means of the luciferin-luciferase assay. The ATP concentration in the light-sensitive growing zone increases 30 to 50% within 30 seconds after the start of a light stimulus and returns to the normal adapted level within 1 minute after stimulation. The ATP concentration is constant for any level of light adaptation and is uniform along the length of sporangiophores even though the light sensitivity is confined to a growing zone less than 5 mm long. These results suggest that one of the initial biochemical steps after a light stimulus is the production of extractable ATP.

Adenosine Triphosphate↗
PubMed1983

Rapid diagnosis of bacteraemia by measuring bacterial adenosine triphosphate in blood culture bottles using bioluminescence.

Bacterial adenosine triphosphate (ATP) was determined in blood culture bottles using bioluminescence. Seventy bottles were inoculated with blood and bacteria. Immediately after inoculation and every 2 h thereafter for the next 10 h, bacterial ATP was measured as well as the number of colony-forming units (CFU) per millilitre of blood culture bottle. The curves for the concentration of CFUs and for the amount of bacterial ATP present are quite similar and indicate that the method described promises good results in the early detection of bacteria in blood culture bottles. ATP values greater than 0.1 ng/ml blood culture bottle indicate bacterial growth. This limit of detection is reached at a concentration of 4-6 X 10(4) CFU/ml of the Escherichia coli ATCC 11229 strain tested.

Adenosine Triphosphate↗
PubMed1993

Perfusion pressure control by adenosine triphosphate given during cardiopulmonary bypass.

Administration of exogenous adenosine triphosphate (ATP) as a vasodilator during cardiopulmonary bypass was assessed in consecutive adult patients (n = 24) who demonstrated a high arterial perfusion pressure (mean, > 90 mm Hg). The action of ATP was characterized by rapid induction and stabilization of the blood pressure level. The dose of ATP ranged from 0.68 to 2.68 mg/min. Within 1 minute after the administration, there was a significant reduction in the perfusion pressure from 102 +/- 18 mm Hg (mean +/- standard deviation) to 72 +/- 19 mm Hg. The ATP was then able to maintain the desired pressure of 69 +/- 12 mm Hg at 5 minutes, 67 +/- 12 mm Hg at 10 minutes, and consistent values thereafter. After the ATP administration was discontinued, there was a prompt recovery of pressure without bradyarrhythmia. The frequency and amount of inotropes used were consistent with the control group (n = 26). Although the administration of ATP reduced the increase in serum catecholamine concentration, there were no significant changes in other vasoactive mediators (eicosanoid, angiotensin II, endothelin) between the two groups during cardiopulmonary bypass. There was neither an accumulation of metabolic products (uric acid, phosphate) nor a decrease in the level of divalent cation (Ca2+), which is observed when the cations combine with phosphates or adenosine nucleotides. This study confirmed the efficacy and safety of ATP infusion during cardiopulmonary bypass.

Adenosine Triphosphate↗
PubMed1999

On-line measurement of adenosine triphosphate and catecholamine released from adrenal chromaffin cells.

Adenosine triphosphate (ATP) and catecholamine (CA) released from cultured porcine adrenal chromaffin cells were continuously measured with an ATP photometer (luciferin-luciferase method) and electrochemical detector, respectively. Application of acetylcholine (ACh, 0.1 mM) or high K+ (60 mM) caused increases of ATP and CA in perfused effluent with the same time course. The peak molar ratio of CA to ATP in the effluent was about 10 for ACh and high K+ stimulation. The high-performance liquid chromatographic (HPLC) analysis of adenine nucleotides in the collected effluent revealed that the relative amounts of ATP, ADP and AMP were almost the same throughout the period of stimulation, suggesting that ATP breakdown in the effluent was constant. Changes in the peak molar ratio of CA to ATP appearing in the effluent did not occur with repetitive high K+ or sustained Ba2+ stimulation (5 mM). The similarity between the time courses of ATP and CA appearing in the effluent suggests that releasable chromaffin granules have a constant molar ratio of CA to ATP. The on-line system developed is a simple and rapid method for examining ATP and CA secretion, simultaneously.

Acetylcholine↗
PubMed2006

Potential use of the adenosine triphosphate cell viability assay in endometrial cancer.

OBJECTIVE: Adenosine triphosphate cell viability assay (ATP-CVA) was used previously to evaluate chemotherapy in uterine cancer cell lines. In this study, we have performed the ATP-CVA on endometrial cancer patients to study the feasibility of using ATP-CVA in endometrial cancer to determine the intrinsic chemosensitivity of the cytotoxic drugs. METHODS: Thirty-three patients with endometrial adenocarcinoma who presented for a staging operation were recruited. Endometrial cancer samples were obtained at the time of operation. In vitro ATP-CVA and chemosensitivity testing was performed using cisplatin, carboplatin, paclitaxel, etoposide, doxorubicin, 4-epidoxorubicin, and topotecan. RESULTS: Thirty-two of the 33 endometrial cancer samples were evaluable for SF50 (survival fraction at 50% of the peak plasma concentration [PPC]) using ATP-CVA. The median SF50 of carboplatin (0.33) was significantly less than the median SF50 of cisplatin (0.71), topotecan (0.93), paclitaxel (0.68), doxorubicin (1.0), etoposide (0.70), or 4-epidoxorubicin (0.88) (Wilcoxon signed rank test, P <.001). CONCLUSION: This study showed the feasibility of using the ATP-CVA in endometrial cancer to determine the intrinsic chemosensitivity of cytotoxic drugs.

Adenocarcinoma↗