Cerebral high-energy compounds: changes in anoxia

1962 ◽  
Vol 202 (1) ◽  
pp. 77-79 ◽  
Author(s):  
Richard N. Lolley ◽  
Frederick E. Samson
Keyword(s):  
Ion Exchange ◽  
Rat Brain ◽  
Adenosine Triphosphate ◽  
Energy Flow ◽  
Inorganic Phosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Guanosine Triphosphate ◽  
Inosine Monophosphate ◽  
Flow Through

Acid-soluble phosphates of rat brain during anoxia were determined by ion-exchange and chemical procedures. There is a general shift during anoxia of triphosphate nucleotides to monophosphates and a very rapid breakdown of phosphoryl-creatine. However, total phosphate leaving the high-energy phosphate pool is not equal to the changes in inorganic phosphate; inorganic phosphate change is much larger than high-energy phosphate change in early anoxia and much smaller in extended anoxia. The patterns of guanosine triphosphate and uridine triphosphate changes are more complex than adenosine triphosphate changes. Nicotinamideadenine dinucleotide levels are steady until late anoxia, at which time they decrease slightly. Cytidine monophosphate is the only cytidine nucleotide detected. Inosine nucleotide concentrations in control animals were below the limit of the method, but in late anoxia inosine monophosphate appeared. The data show that the energy flow through the phosphates in brain is rapid and involves phosphate compounds other than the acid-soluble nucleotides and phosphoryl-creatine.

High Energy Phosphates During Hibernation and Arousal in the Ground Squirrel

1958 ◽  
Vol 195 (1) ◽  
pp. 233-236 ◽  
Author(s):  
Marilyn L. Zimny ◽  
Roy Gregory
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Adenosine Triphosphate ◽  
Ground Squirrel ◽  
Inorganic Phosphate ◽  
Liver Glycogen ◽  
High Energy ◽  
Ground Squirrels ◽  
High Energy Phosphates ◽  
High Energy Phosphate

Biochemical levels of inorganic phosphate, adenosine triphosphate, phosphocreatine and glycogen were determined on cardiac muscle, skeletal muscle and liver samples from hibernated 13-striped ground squirrels and those allowed to awaken for intervals of 7.5, 15 and 30 minutes. Cardiac muscle glycogen increases during hibernation apparently at the expense of skeletal muscle and liver glycogen. Glycolysis occurs in these tissues during early arousal, followed later by glycogenesis. Adenosine triphosphate is maintained in both cardiac and skeletal muscle during hibernation and is used as an energy source during arousal. It appears that glycolysis is important in resynthesizing phosphocreatine. From this study of periods of relatively low and high metabolic demands we conclude that phosphocreatine is a ‘transport’ form of high-energy phosphate forming adenosine triphosphate from the phosphate pool when and where needed in the cycle of intermediary metabolism.

Cellular K+ loss and anion efflux during myocardial ischemia and metabolic inhibition

1989 ◽  
Vol 256 (4) ◽  
pp. H1165-H1175 ◽  
Author(s):  
J. N. Weiss ◽  
S. T. Lamp ◽  
K. I. Shine
Keyword(s):  
Inorganic Phosphate ◽  
Lactate Production ◽  
Selective Inhibition ◽  
High Energy ◽  
Metabolic Inhibitors ◽  
Charge Movement ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Myocardial Hypoxia ◽  
Inhibition Of Glycolysis

It has been suggested that increased K+ efflux during myocardial hypoxia and ischemia may result from efflux of intracellularly generated anions such as lactate and inorganic phosphate (Pi) as a mechanism of balancing transsarcolemmal charge movement. To investigate this hypothesis cellular K+ loss using 42K+ and K+-sensitive electrodes, intracellular potential, venous lactate and Pi, and tissue lactate and high-energy phosphates were measured in isolated arterially perfused rabbit interventricular septa during exposure to metabolic inhibitors, hypoxia, and ischemia. Selective inhibition of glycolysis caused a marked increase in K+ efflux despite a fall in lactate production and maintenance of normal cellular high-energy phosphate content. During ischemia and hypoxia net loss of lactate and Pi exceeded K+ loss by a factor of 2-6. However, removal of glucose prior to ischemia or during hypoxia increased K+ loss but reduced lactate loss without affecting Pi loss. During hypoxia, 30 mM exogenous lactate did not alter K+ loss in a manner consistent with changes in passive electrodiffusion of lactate ion. These findings inhibition which is not related to anion efflux assumes greater importance under conditions in which glycolysis is inhibited, e.g., ischemia. Under conditions in which glycolysis is not inhibited, e.g., hypoxia, K+ efflux does not parallel passive electrodiffusion of lactate ions. However, this finding does not exclude the possibility that K+ loss could be coupled to carrier-mediated lactate ion efflux.

Control mechanisms in blood fluidity: role of adenosine triphosphate

1963 ◽  
Vol 18 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
L. O. Pilgeram ◽  
D. A. Loegering
Keyword(s):  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
High Energy ◽  
Control Mechanisms ◽  
High Energy Phosphate ◽  
Cellular Mechanisms ◽  
Blood Fluidity ◽  
Phosphate Linkage ◽  
Glass Surfaces

A possible role for cellular energy metabolism in the control of the blood clotting mechanism has been shown. High-energy phosphate was found to strongly inhibit the recalcification time of plasma prepared with siliconized or glass surfaces. The nucleotide, adenosine triphosphate, in crystalline form and chromatographically pure, will inhibit or completely prevent coagulation in vitro. Reactivity is based primarily on the high-energy phosphate linkage and secondarily upon the nucleoside, adenosine. The principal site of action for ATP is on an unidentified precursor of thromboplastin. Available evidence indicates an important role for energy metabolism in the cellular mechanisms which effect a control over thromboplastin generation and its possible thrombotic and arteriosclerotic sequelae. cellular control mechanisms; blood fluidity; thrombosis arteriosclerosis; aging Submitted on July 1, 1963

Bioenergetics of acute vasogenic edema

1980 ◽  
Vol 53 (4) ◽  
pp. 470-476 ◽  
Author(s):  
Leslie N. Sutton ◽  
Frank Welsh ◽  
Derek A. Bruce
Keyword(s):  
White Matter ◽  
Adenosine Triphosphate ◽  
Vasogenic Edema ◽  
Lactate Concentration ◽  
High Energy ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Content Type ◽  
Cold Lesion ◽  
Fine Print

✓ The bioenergetic mechanisms of vasogenic edema were studied by measuring concentrations of adenosine triphosphate (ATP), phosphocreatine (CrP), and lactate in rapidly frozen edematous white matter in cats. When edema was produced using a cold lesion, it was found that both ATP and CrP were reduced to one-half of control values, and that lactate was elevated. When a correction was applied for dilution, however, it was found that high-energy phosphates were equal to control values, and that lactate was even more significantly elevated. This pattern contrasted with that seen in white-matter ischemia, in which CrP is depressed out of proportion to ATP. Finally, it was found that the white-matter lactate concentration in the plasma infusion model of edema was increased. It is concluded that vasogenic edema induces an increase in lactate, but does not deplete high-energy phosphate compounds in affected white matter.

INFLUENCES OF THYROXINE AND INSULIN ON THE TURNOVER AND FATE OF HIGH-ENERGY PHOSPHATE

1964 ◽  
Vol 42 (6) ◽  
pp. 777-786 ◽  
Author(s):  
Dorothy S. Dow
Keyword(s):  
Skeletal Muscle ◽  
Energy Transfer ◽  
Adenosine Triphosphate ◽  
Cell Structure ◽  
Adenosine Diphosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Nucleoside Phosphorylase ◽  
Mitochondrial Permeability ◽  
Energy Acceptor

Ingestion by the weanling rat of thyroxine in an amount greatly in excess of physiological requirements resulted in significant increases in the rates of turnover of the high-energy compounds phosphocreatine (PC), adenosine diphosphate (ADP), and adenosine triphosphate (ATP) and in significant decreases in their concentrations in skeletal muscle. Nucleoside phosphorylase and myokinase activities and rates of pyrophosphate splitting of ATP and of utilization of ATP for nuclear syntheses were unaltered in thyrotoxic muscle. The findings suggest that increased extramitochondrial utilization of ATP for glycolysis may be the factor responsible for the increased phosphorylating capacity of the thyrotoxic animal. An effect of thyroxine on mitochondrial permeability as well as on rate of formation of the high-energy intermediate would appear to explain the observed results.A further enhancement of the already markedly elevated thyrotoxic rate of phosphorylation was effected by the superimposition of insulin. Insulin also effected increases in the concentrations of the high-energy compounds. It is apparent that insulin acts by reducing the utilization of ATP for phosphorylation of glucose and thus increases the mitochondrial availability of high-energy acceptor. This increased mitochondrial affinity for high-energy compounds results in an enhancement of mitochondrial energy transfer processes.The findings appear to involve both thyroxine and insulin in the control of cell structure.

Myocardial high-energy phosphate metabolism is altered after treatment with anthracycline in childhood

2000 ◽  
Vol 10 (6) ◽  
pp. 610-617 ◽  
Author(s):  
Andrea B. Eidenschink ◽  
Gerrit Schröter ◽  
Stefan Müller-Weihrich ◽  
Heiko Stern
Keyword(s):  
Adenosine Triphosphate ◽  
High Energy ◽  
Left Ventricular ◽  
Control Group ◽  
Left Ventricular Myocardium ◽  
Resonance Spectroscopy ◽  
Phosphate Metabolism ◽  
High Energy Phosphate ◽  
High Energy Phosphate Metabolism

AbstractObjectivesWe aimed to investigate whether changes in high-energy phosphate metabolism after treatment of children and young adults with anthracycline can be demonstrated non-invasively by 31P magnetic resonance spectroscopy.BackgroundAbnormal myocardial energy metabolism has been suggested as a mechanism for anthracycline-induced cardiotoxicity. Deterioration in such has been shown in animal studies by resonance spectroscopy.MethodsWe studied 62 patients, with a mean age of 13.5 ±5 years,3.7±4.3 years after a cumulative anthracycline dose of 270±137 mg/m2. Normal echocardiographic findings had been elicited in 54 patients. The control group consisted of 28 healthy subjects aged 20±7 years. Resonance spectrums of the anterior left ventricular myocardium were obtained at 1.5 Tesla using an image-selected in vivo spectroscopy localization technique.ResultsThe ratio of phosphocreatine to adenosine triphosphate after blood correction was 1.09±0.43 for the patients, and 1.36±0.36 (mean±SD)for controls (p = 0.005), with a significantly reducedmean ratio even in the subgroup of patients with normal echocardiographic results ( l.11 ± 0. 44 versus1.36±0.36, p=0.01). The ratio did not correlate with the cumulative dose of anthracycline. The ratio of phosphodiester to adenosine triphosphate was similar in patients and controls (0.90±0.56 versus 0.88±0.62).ConclusionsIn patients treated with anthracyclines in childhood, myocardial high-energy phosphate metabolism may be impaired even in the absence of cardiomyopathy. Our data support the concept that anthracycline-induced cardiotoxicity is not clearly dose dependent.

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