STUDIES ON MYOFIBRILLAR ADENOSINE TRIPHOSPHATASE WITH CALCIUM-FREE ADENOSINE TRIPHOSPHATE.
Explore the source record for details and available documents.
Adenosine Triphosphatases↗
SEARCH · Search PubMed
Results for “ADENOSINE TRIPHOSPHATE”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
A Trypanosoma cruzi heat shock protein 40 is able to stimulate the adenosine triphosphate hydrolysis activity of heat shock protein 70 and can substitute for a yeast heat shock protein 40.
The process of assisted protein folding, characteristic of members of the heat shock protein 70 (Hsp70) and heat shock protein 40 (Hsp40) molecular chaperone families, is important for maintaining the structural integrity of cellular protein machinery under normal and stressful conditions. Hsp70 and Hsp40 cooperate to bind non-native protein conformations in a process of adenosine triphosphate (ATP)-regulated assisted protein folding. We have analysed the molecular chaperone activity of the cytoplasmic inducible Hsp70 from Trypanosoma cruzi (TcHsp70) and its interactions with its potential partner Hsp40s (T. cruzi DnaJ protein 1 [Tcj1] and T. cruzi DnaJ protein 2 [Tcj2]). Histidine-tagged TcHsp70 (His-TcHsp70), Tcj1 (Tcj1-His) and Tcj2 (His-Tcj2) were over-produced in Escherichia coli and purified by nickel affinity chromatography. The in vitro basal specific ATP hydrolysis activity (ATPase activity) of His-TcHsp70 was determined as 40 nmol phosphate/min/mg protein, significantly higher than that reported for other Hsp70s. The basal specific ATPase activity was stimulated to a maximal level of 60 nmol phosphate/min/mg protein in the presence of His-Tcj2 and a model substrate, reduced carboxymethylated alpha-lactalbumin. In vivo complementation assays showed that Tcj2 was able to overcome the temperature sensitivity of the ydj1 mutant Saccharomyces cerevisiae strain JJ160, suggesting that Tcj2 may be functionally equivalent to the yeast Hsp40 homologue (yeast DnaJ protein 1, Ydj1). These data suggest that Tcj2 is involved in cytoprotection in a similar fashion to Ydj1, and that TcHsp70 and Tcj2 may interact in a nucleotide-regulated process of chaperone-assisted protein folding.
Adenosine Triphosphatases↗
Improved ischemic island skin flap survival with continuous intraarterial infusion of adenosine triphosphate--magnesium chloride and superoxide dismutase: a rat model.
Neurovascular island skin flaps are still hampered by occasional necrosis of their most distal aspect. Cells subjected to prolonged hypoxic conditions become intracellularly depleted of needed metabolic substrates and eventually die. Once hypoxic conditions are improved, ischemic tissue suffers further injury from the rapid accumulation of oxygen free radicals. This study showed 53% survival of a standard random flap constructed on the inferior epigastric neurovascular bundle of a rat. Random flap survival increased to 65% after intraarterial infusion of adenosine triphosphate--magnesium chloride (ATP-MgCl2); to 75% after superoxide dismutase infusion; and to 98% after combined ATP-MgCl2 and superoxide dismutase infusion. Neither substrate appeared to act by increasing blood flow to the ischemic tissue.
Adenosine Triphosphate↗
Bioluminescence assay of adenosine triphosphate in drug susceptibility testing of Mycobacterium tuberculosis.
Twenty three clinical isolates M. tuberculosis and the reference strain, M. tuberculosis H37Rv were tested for their susceptibility to trifluoperazine (TFP) by the standard broth dilution method and the bioluminescence assay. The results showed that in 15 of the 23 isolates, the minimal inhibitory concentration (MIC) was identical in both the methods and in the remaining 8 isolates the difference in the MIC values between the methods, was less than two fold and was not significant. The findings suggest that the measurement of adenosine triphosphate (ATP) by bioluminescence assay can be employed as an alternative method for the rapid screening of clinical isolates for their susceptibility to anti-mycobacterial agents.
Adenosine Triphosphate↗
Fetal exposure to magnesium chloride-adenosine triphosphate (MgCl2-ATP) results in alterations in cerebral blood flow and a metabolic acidosis.
OBJECTIVE: Magnesium chloride-adenosine triphosphate (MgCl(2)-ATP), advocated as an adjunct treatment in shock resuscitation, might be useful for pregnant women who develop hypovolemia secondary to conditions such as placental abruption. The effects of this treatment on the fetus, however, have never been investigated. This study determined the direct, acute effects of MgCl(2)-ATP on fetal organ blood flow, hemodynamic measurements, and metabolic parameters before and after maternal hemorrhage. DESIGN: Experimental, randomized, nonblinded, control study. SETTING: Animal laboratory at a university research facility. SUBJECTS: This study was performed on 11 chronically instrumented, 123-day gestational age, pregnant ewes (term = 147 days) and their fetuses. INTERVENTIONS: Ewes were randomly allocated to either experimental (Expt, n = 5) or control (Cntl, n = 6) groups. After a 60-min baseline period, Expt fetuses received a 60-min iv infusion of MgCl(2)-ATP (150 &mgr;mole/hr each of MgCl(2) and ATP; at 3 mL/hr), and Cntl fetuses received an equivalent volume of 0.9% NaCl. After this infusion-only period, the infusion was continued, and ewes were intermittently bled over 1 hr for a total blood loss of 20 mL/kg (hemorrhage-plus-infusion period). After this, the infusions were continued, and ewes and fetuses were monitored for 1 additional hr (posthemorrhage period). Measurements: At the end of all periods, fetal and maternal blood pressures, blood gases, oxygen saturation, hemoglobin, serum electrolytes, and serum glucose concentrations were measured. At the end of the baseline, infusion-only, and hemorrhage-plus-infusion periods, fetal organ blood flows were determined using a fluorescent microsphere technique. Nonparametric statistics were used for comparisons (2-tailed, p </=.05). MAIN RESULTS: Maternal hemorrhage caused maternal hypotension, resulting in a decrease in fetal oxygen content and an increase in fetal hemoglobin and glucose concentrations. The changes were similar in both groups. In both groups, a progressive fetal metabolic acidosis developed during the hemorrhage period and it continued through the posthemorrhage period. This metabolic acidosis was more severe in the Expt fetuses and appeared to have started during the infusion-only period. There were no fetal deaths in either group. In the Cntl fetuses, there were increases from baseline after the hemorrhage-plus-infusion period in fetal adrenal (71%), brain (89%), and thymus (18%) blood flow and a decrease in muscle (-28%) blood flow. In the Expt fetuses, there were increases during the infusion-only period in adrenal (332%), myocardial (142%), and pancreatic (219%) blood flow and decreases in kidney (-25%) and skin (-75%) blood flow. These changes persisted during the hemorrhage-plus-infusion period. Most strikingly, regional cerebral blood flow in the Expt fetuses did not increase from baseline in any of the 10 brain areas sampled during the infusion-only period or following maternal hemorrhage. In Cntl fetuses, however, there was increase in blood flow in all 10 brain areas sampled following maternal hemorrhage. CONCLUSIONS: In healthy fetuses, direct MgCl(2)-ATP exposure caused metabolic acidosis and a redistribution of cardiac output to different organs. When the MgCl(2)-ATP fetuses were then subject to the effects of maternal hemorrhage, the expected increase in cerebral blood flow was not observed. Although an earlier study suggests that ATP may be beneficial to stressed fetuses when administered to mothers in labor, the direct effect of MgCl(2)-ATP appears to be potentially harmful by producing an acidosis and altering the normal fetal cerebral blood flow response to maternal hemorrhage.
Journal Article↗
The effect of phenazine methosulfate-ascorbate on bacterial active transport and adenosine triphosphate formation: inhibition of Pseudomonas aeruginosa and stimulation of Escherichia coli.
The artificial electron-donor system, phenazine methosulfate (PMS) ascorbate, inhibited active transport of glucose by Pseudomonas aeruginosa irrespective of whether the incubation systems were in air, flushed with oxygen, or gassed with nitrogen under anaerobic denitrifying conditions. Active transport of glucose by P. aeruginosa was also inhibited by reduced 5-N-methyl-phenazonium-3-sulfonate, a membrane-impermeable electron donor. PMS-ascorbate caused rapid depletion of intracellular adenosine triphosphate (ATP) when added to respiring cell suspensions of P. aeruginosa either in the presence or absence of glucose or succinate as oxidizable energy sources. In contrast, under identical conditions, Escherichia coli formed ATP with PMS-ascorbate as the sole oxidizable energy source and ATP formation continued when glucose or succinate was present in addition to PMS-ascorbate in the incubation system.
Adenosine Triphosphate↗
Assessment of myocardial perfusion by harmonic power doppler imaging at rest and during adenosine triphosphate stress: comparison with coronary flow velocity reserve in the left anterior descending coronary arter.
To clarify whether the myocardial perfusion abnormalities observed on harmonic power Doppler imaging (HPDI) during hyperemia are related to a decrease in coronary flow velocity reserve (CFVR), HPDI and CFVR were measured in the left anterior descending coronary artery (LAD) territory of 75 patients. During continuous infusion of Levovist, dual-frame triggered apical 4-chamber views were obtained at rest and during adenosine triphosphate (ATP) infusion. The persistence of perfusion defects during ATP infusion or stress-induced defects in the LAD territory was defined as abnormal. Both HPDI and coronary flow velocity recordings of adequate quality were successfully obtained in 73 patients, and 37 patients showed abnormal myocardial perfusion. CFVR was significantly lower in patients with abnormal perfusion than in patients who had normal findings (1.38+/-0.38 vs 2.60+/-0.76, p<0.001). A CFVR less than 1.9 had a sensitivity of 89% (33/37) and a specificity of 89% (32/36) for predicting the presence of abnormal myocardial perfusion. This study demonstrates that myocardial perfusion abnormalities observed during HPDI using ATP stress are closely correlated to a decrease in CFVR and may reflect significant stenosis or microvascular damage in the LAD territory.
Adenosine Triphosphate↗
Bile-induced adenosine triphosphate depletion and mucosal damage during reflux esophagitis.
BACKGROUND: This study was designed to investigate the role of bile in a large animal model of acute esophageal reflux disease. METHODS: An agar electrode was used to measure the transmucosal potential difference of the esophagus in anaesthetized dogs. The vascular permeability index and the epithelial permeability index of the mucosa were evaluated by means of the Evans blue and the sodium-fluorescein clearance method, respectively. The tissue adenosine triphosphate (ATP) level and the myeloperoxidase activity were determined from tissue biopsies, while the degree of mucosal damage was evaluated histologically on a grade 0-100 scale. Group 1 (n = 8) served as saline-treated control; groups 2 (n = 8), 3 (n = 5) and 4 (n = 5) were exposed for 4 h to canine bile alone, to hydrochloric acid + bile, or to hydrochloric acid alone, respectively. RESULTS: In Groups 2, 3 and 4 the degree of mucosal damage was significantly increased, and a 4-fold elevation in myeloperoxidase activity was observed. The transmucosal potential difference was decreased significantly below the control level, while the vascular and epithelial permeability indices were significantly increased compared with the control values. Bile, but not hydrochloric acid, evoked a significant (40%) decrease in the ATP level of the esophageal tissue. CONCLUSIONS: We propose that mucosal dysfunction, structural damage and leukocyte invasion during hydrochloric acid-induced esophageal injury are exacerbated by bile-induced changes in tissue ATP concentrations during experimental esophageal reflux disease.
Acute Disease↗
Prevention of intracellular adenosine triphosphate depletion after sublethal oxidant injury to rat type II alveolar epithelial cells with exogenous glutathione and N-acetylcysteine.
The alveolar epithelial cells of the lower respiratory tract are exposed continuously to injurious agents, including oxygen radicals. The type II alveolar epithelial cell is critically important to the normal function of the lung, because it is responsible for synthesis of surfactant and other essential duties. In the current investigation, the authors documented the loss of intracellular adenosine triphosphate (ATP) after exposure of the cells to sublethal concentrations of hydrogen peroxide (H2O2) and hypochlorous acid. Subsequent experiments attempted to alleviate or prevent this oxidant mediated loss of ATP by preincubating the cells with either glutathione or N-acetylcysteine (NAC). Initially, it was determined that exposure of the type II cells to 250 microM hypochlorous acid or 250 microM H2O2 for 1 hour each would cause significant loss of type II cell ATP. However, preincubation with glutathione (1,000 microM) inhibited the loss of ATP after both exposure to 250 microM H2O2 (24 +/- 3% loss of ATP without glutathione compared with 13 +/- 2% loss with glutathione, P < 0.05), and 250 microM hypochlorous acid (12 +/- 2% loss of ATP without glutathione compared with 1 +/- 1% increase of ATP with glutathione). Similar results were obtained using NAC (2 mg/mL) after exposure to 250 microM H2O2 (23 +/- 2% loss of ATP without NAC compared with a 4 +/- 3% loss of ATP with NAC). This study demonstrates that exogenous glutathione and NAC are able to protect type II cells from oxidant mediated sublethal injury and loss of intracellular ATP stores.
Acetylcysteine↗
Muscle contractures and adenosine triphosphate depletion in porcine malignant hyperthermia.
This study compares several methods for diagnosing susceptibility to malignant hyperthermia, using two groups of Poland China swine narrowly defined as genetically susceptible or normal (five pigs each) depending respectively on their response to halothane or to halothane and succinylcholine. Vastus medialis muscle biopsies were excised under thiopental-N2O-O2 anesthesia and used for examination of (1) contracture responses to halothane, (2) contracture responses to caffeine and halothane-caffeine, and (3) adenosine triphosphate (ATP) depletion with and without halothane. All studies were performed in organ baths at 37 C. Halothane alone produced contractures in two susceptible and one normal preparation; caffeine always produced a contracture at lower concentrations in susceptible muscle; caffeine-halothane contractures in susceptible muscle occurred at lower mean caffeine concentrations, but there was some overlap of individual values; mean ATP depletion was greater in susceptible muscle, but with considerable overlap. Comparisons with the findings of others were hampered by use of absolute rather than comparative values for tension, e.g., grams, rather than grams per cross-sectional area or fraction of peak tension. Examination of the complete dose-response curve provided the best comparative information and caffeine was the consistent predictor of susceptibility.
Adenosine Triphosphate↗
Effect of chronic denervation on the activities of monoamine oxidase and catechol-O-methyl transferase and on the contents of noradrenaline and adenosine triphosphate in the rabbit ear artery.
When assayed on homogenates of the rabbit ear artery up to 192 h after sympathetic denervation, the activity of monoamine oxidase (MAO) showed a small but significant decrease (maximum 9%). The activity of catechol-O-methyl transferase (COMT) appeared unchanged, although it is possible that the small and variable nature of this enzyme activity compared with that of MAO may have masked a comparable effect of denervation. The maximum decreases in noradrenaline (NA) and adenosine triphosphate (ATP) contents were greater than 90% at 48 h, and 32% at 96 h after denervation. These results confirm the presence of neuronal as well as extra-neuronal MAO, and also the presence of extraneuronal comt in this artery. The decline in ATP contents after denervation suggest that part of the ATP is neuronal. However, the estimated ratio of NA to neuronal ATP is far in excess of that reported for isolated noradrenaline storage vesicles, suggesting that the major portion of the neuronal ATP was not present in these vesicles.
Adenosine Triphosphate↗
Enhanced biological phosphorus removal from wastewater by biomass with different phosphorus contents, Part II: Anaerobic adenosine triphosphate utilization and acetate uptake rates.
Data from laboratory-scale sequencing batch reactors operated in an anaerobic-aerobic cycle showed that a low influent phosphorus/chemical oxygen demand (COD) ratio feed favored a glycogen-accumulating metabolism (GAM)-dominated culture and that a high influent phosphorus/COD ratio feed favored a polyphosphate-accumulating metabolism (PAM)-dominated culture. The PAM-dominated culture anaerobically took up acetate approximately 7 times faster than the GAM-dominated culture. Adenosine triphosphate (ATP) balances were performed assuming eight different metabolic scenarios that included the Entner-Doudoroff or the Embden-Myerhof glycolytic pathway, acetyl-coenzyme A (CoA) synthase or the acetate kinase-phospho-transacetylase (AK-PTA) system for acetyl-CoA synthesis, and ATP synthesis or no ATP synthesis during fumarate reduction. The ATP available for transport of acetate into the cell (2) was calculated using these balances. The assumed quantity of ATP produced during fumarate reduction had a relatively small effect on alpha, particularly when PAM was dominant. When GAM was dominant, little or no ATP was available for acetate transport depending on the assumed scenario, and the Embden-Myerhof pathway was more feasible. The value of alpha increased with increasing PAM dominance for all eight metabolic pathways. The maximum calculated alpha value of 0.5 mol ATP/C-mol acetate uptake occurred at maximum PAM dominance and when the Embden-Myerhof pathway was active, when ATP was produced during fumarate reduction, and when the AK-PTA system was active. This value of alpha was higher than previously calculated values with the same metabolic assumptions. An acetate uptake mechanism was suggested that included acetyl-CoA synthetase and direct regeneration of the proton motive force by a proton-translocating pyrophosphatase. Polyphosphate-accumulating metabolism may have a competitive advantage over GAM through a higher anaerobic acetate uptake rate made possible by a greater use of energy for acetate uptake, by use of a different acetate uptake mechanism, or both.
Acetate-CoA Ligase↗
Dual effect of adenosine triphosphate on the apical small conductance K+ channel of the rat cortical collecting duct.
We used the patch-clamp technique to study the effects of ATP on the small-conductance potassium channel in the apical membrane of rat cortical collecting duct (CCD). This channel has a high open probability (0.96) in the cell-attached mode but activity frequently disappeared progressively within 1-10 min after channel excision (channel "run-down"). Two effects of ATP were observed. Using inside-out patches, low concentrations of ATP (0.05-0.1 mM) restored channel activity in the presence of cAMP-dependent protein kinase A (PKA). In contrast, high concentrations (1 mM) of adenosine triphosphate (ATP) reduced the open probability (Po) of the channel in inside-out patches from 0.96 to 0. 1.2 mM adenosine diphosphate (ADP) also blocked channel activity completely, but 2 mM adenosine 5'-[beta,gamma-imido]triphosphate (AMP-PNP), a nonhydrolyzable ATP analogue, reduced Po only from 0.96 to 0.87. The half-maximal inhibition (Ki) of ATP and ADP was 0.5 and 0.6 mM, respectively, and the Hill coefficient of both ATP and ADP was close to 3. Addition of 0.2 or 0.4 mM ADP shifted the Ki of ATP to 1.0 and 2.0 mM, respectively. ADP did not alter the Hill coefficient. Reduction of the bath pH from 7.4 to 7.2 reduced the Ki of ATP to 0.3 mM. In contrast, a decrease of the free Mg2+ concentration from 1.6 mM to 20 microM increased the Ki of ATP to 1.6 mM without changing the Hill coefficient; ADP was still able to relieve the ATP-induced inhibition of channel activity over this low range of free Mg2+ concentrations. The blocking effect of ATP on channel activity in inside-out patches could be attenuated by adding exogenous PKA catalytic subunit to the bath. The dual effects of ATP on the potassium channel can be explained by assuming that (a) ATP is a substrate for PKA that phosphorylates the potassium channel to maintain normal function. (b) High concentrations of ATP inhibit the channel activity; we propose that the ATP-induced blockade results from inhibition of PKA-induced channel phosphorylation.
Adenosine Diphosphate↗
The conductance of cultured epithelial cell monolayers: oxidants, adenosine triphosphate, and phorbol dibutyrate.
Oxidants are one class of inflammatory molecules that may contribute to an increase in epithelial permeability to water and solutes that commonly occurs during acute inflammation. We and others have observed that oxidants reversibly alter the paracellular conductance of Madin Darby canine kidney epithelial (MDCK) cell monolayers. The mechanism by which oxidants reversibly alter MDCK monolayer conductance is not yet fully understood. Some investigators have suggested that oxidants might alter MDCK monolayer paracellular conductance by depleting adenosine triphosphate (ATP) in the cells. When we exposed MDCK cells to doses of oxidants that increased monolayer paracellular conductance in earlier studies, ATP was depleted within 10 min. However, when ATP was depleted to similar levels with an inhibitor of glycolytic ATP production, 2-deoxy-D-glucose (DOG), monolayer paracellular conductance was not increased. Severe ATP depletion with DOG and the mitochondrial metabolic inhibitor, antimycin A (AA), had very limited, ATP-independent effects on paracellular conductance. As an alternative explanation for the effects of oxidants on MDCK monolayer paracellular conductance, we had reported that oxidants increased production of inositol phosphates and diglycerides in MDCK cells. Synthetic diglyceride and phorbol dibutyrate (PDBU) increased MDCK monolayer conductance to ions and mannitol in earlier studies. When MDCK cell ATP was depleted with DOG (to the level caused by oxidants), the increase in conductance following PDBU was not different from that observed in control cells. More severe ATP depletion, with DOG and AA, prevented the increase in conductance following PDBU.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗
Adenosine triphosphate modification of endotoxin-induced otitis media with effusion in gerbils.
BACKGROUND: Impairment of the mucociliary system of the middle ear epithelium is a key step in developing otitis media with effusion. Effective propulsion of the viscoelastic gel layer of mucus requires a control of the depth of the periciliary sol layer by means of epithelial ion transport. In a previous study, we successfully demonstrated modulation of ion transport via short-circuit current changes by specific stimulation of adenosine triphosphate (ATP) receptors in a middle ear cell line. MATERIALS AND METHODS: Otitis media with effusion was developed in gerbils by infusing Escherichia coli E.coli lipopolysaccaride. In group A, E. coli lipopolysaccharide was first infused, and after establishment of middle ear fluid, the right ear was infused with 10(-4) M ATP, while the left ear remained as the control. In group B, the right ear was infused first with 10(-4) M ATP followed by bilateral infusion with endotoxin. The morphology of the middle ear mucosa was studied using scanning electron microscopy (SEM). RESULTS: Group A showed fluid clearance in 5 out of 15 ATP-treated right ears while 3 out of 15 left ears showed clearance. Group B showed persistent presence of fluid in 11 out of 15 ATP-treated right ears, while the left ears showed fluid in 13 out of 15. SEM study consistently demonstrated scanty cilia in the non-ATP treated ears, but in ATP-treated ears the cilia remained abundant. CONCLUSION: Although the results showed that ATP could not effectively prevent or clear middle ear effusion, the SEM result showed a marked beneficial effect of ATP on preserving ciliary configuration.
Adenosine Triphosphate↗
[The diagnostic and therapeutic usefulness of adenosine triphosphate in supraventricular tachycardias].
The efficacy and safety of intravenous adenosine-5'-triphosphate (ATP) in supraventricular tachycardia (SVT) were investigated in 40 patients, aged 1 month-69 years (mean 28 years). Thirty-one had a history of paroxysmal supraventricular tachycardia (group A), 9 had chronic supraventricular tachycardia (group B). Four patients in Group A had long R-P' tachycardia. In group A, transesophageal atrial pacing was utilized for tachycardia induction. A ventriculoatrial interval (VA) during tachycardia greater than 70 ms was considered diagnostic for reentry by an AV accessory pathway (AP), while a VA less than or equal to 70 ms suggested reentry within the AV node. Serial rapid intravenous injections of graded doses of ATP were performed in both groups. In 14 patients of group A, graded doses of ATP (0.075, 0.1, 0.125, 0.15, 0.2, mg/kg) were performed in order to analyze the dose-response relationships. In group A, ATP resulted in termination of tachycardia in all patients (21 with reentry by an AP, 10 with intranodal reentry). A total of 77 tachycardia episodes were interrupted. A 100% efficacy was found with doses of greater than or equal to 0.15 mg/kg of ATP. Among patients with AP reentry, interruption in the anterograde limb of the reentry circuit occurred in 16 patients, while termination of tachycardia after retrograde block was observed in 5 patients, 4 of whom with long RP' tachycardia. In group B, ATP resulted in transient 2:1 or high degree AV block in 8 patients. Transient restoration of sinus rhythm was observed in 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗
Myocardial adenosine triphosphate content as a measure of metabolic and functional myocardial protection in children undergoing cardiac operation.
In an effort to quantitate the metabolic and functional response to global myocardial ischemia as a prelude to specific interventions to improve myocardial protection in children, the following data were collected. Twenty children (age, 1.16 +/- 0.3 years) underwent repair of congenital intracardiac malformations using aortic cross-clamping and cold potassium cardioplegia (ischemic time, 56.1 +/- 4.5 minutes). Metabolic protection was assessed by measuring the myocardial adenosine triphosphate (ATP) content by microbioluminescence. Before and after ischemia 10-mg myocardial samples were obtained from the left ventricular apex using a Tru-cut biopsy needle. In 15 patients, postoperative ventricular function was measured by radionuclide ventriculography at 72 to 96 hours following operation. Five of 6 patients with a postischemic ATP level less than 40% of control (26.3 +/- 2.8) had a left ventricular ejection fraction (EF) lower than 55% (50.3 +/- 2.3). Seven of 9 patients with an ATP level greater than 40% of the preischemic level (98.0 +/- 14.4) had a normal EF (61.8 +/- 2.9; p less than 0.04). Two other patients with postischemic ATP levels lower than 40% of control died of low cardiac output and had no postoperative ventricular function studies. Thus, of 7 patients with postischemic ATP levels lower than 40% of preischemic levels, 2 died and 5 had depressed left ventricular function. These data support the concept that low postischemic ATP levels correlate with death or poor postoperative ventricular function, and indicate that this variable will be useful to assess future improvements in myocardial protection during pediatric cardiac operations.
Adenosine Triphosphate↗
Embryonic adenosine triphosphate:phosphodiesters ratios obtained with in vivo nuclear magnetic resonance spectroscopy (phosphorus-31): a new technique for selecting leaner broiler chickens.
Phosphorus-containing compounds of 18-d-old embryos from two broiler chicken lines, differing in body fat content, were measured using in vivo 31P nuclear magnetic resonance (NMR) spectroscopy. Subsequently, the same birds were slaughtered at 8 wk of age and the whole body was analyzed for body fat content. The birds of the fat line had lower (P = .002) embryonic adenosine triphosphate (ATP):phosphodiester (PDE) ratios, higher (P = .002) body fat content when adjusted to common BW, and higher (P = .047) dry matter content than the lean line. No differences (P > .05) were detected for BW between the two lines. Females of the two lines had lower (P = .002) ATP:PDE ratios, lower (P = .001) BW, higher (P = .003) adjusted fat contents, and higher (P = .003) dry matter content than the males. No interaction (P > .05) between sexes and lines was detected for any variables. Regression equations indicating a linear negative relationship (Ybody fat content = 369.05 - 407.27 XATP:PDE + .1295 XBW, R2 = .62 to .78; or Ybody fat % = 30.57 - 19.4 XATP:PDE, R2 = .49 to .71) between embryonic ATP:PDE ratios and body fat content were developed.
Adenosine Triphosphate↗