scholarly journals Acquired granular pool defect in stored platelets

Blood ◽  
1981 ◽  
Vol 57 (2) ◽  
pp. 203-208 ◽  
Author(s):  
AK Rao ◽  
S Niewiarowski ◽  
S Murphy
Keyword(s):  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Adenylate Energy Charge ◽  
Platelet Factor ◽  
Final Volume ◽  
Before And After ◽  
Functional Defect ◽  
Metabolic Pool ◽  
The Mean

Abstract Platelets stored as concentrates (PC) for 72 h at 22 degrees C develop a functional defect. Alterations in adenine nucleotides of platelets have been shown to affect platelet function. Adenine nucleotide content of platelets was measured before and after storage and a decrease of 27.1 /+- 1.7% (mean /+- SE) in ATP and 39.1 /+- 2.6% in ADP were found in 34 PC stored with final volume of 50 ml. In 11 PC with 30 ml volume. ATP and ADP decreased by 39.4 /+- 3.2% and 49.4 /+- 2.1%, respectively. The mean ATP to ADP ratio of stored platelets was significantly higher than of fresh platelets in both groups, suggesting a relatively greater decrease in granular than metabolic pool nucleotides. Levels of low affinity platelet factor 4 measured by radioimmunoassay in plasma from 0.86 /+- 0.08 microgram/ml in the fresh PC to 8.59 /+- 0.39 microgram/ml in stored PC, indicating a concomitant alpha-granular secretion. Labeling of metabolic pool with 14C-adenine revealed a mean decrease in the adenylate energy charge of 2.0 /+- 0.4% in 12 of 16 stored PC, with a lower ATP and higher hypoxanthine labeling in stored as compared to fresh platelets. These observations suggest that stored platelets develop an acquired defect in both dense and alpha granules and in their ability to maintain ATP homeostasis.

scholarly journals Acquired granular pool defect in stored platelets

Blood ◽  
1981 ◽  
Vol 57 (2) ◽  
pp. 203-208
Author(s):  
AK Rao ◽  
S Niewiarowski ◽  
S Murphy
Keyword(s):  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Adenylate Energy Charge ◽  
Platelet Factor ◽  
Final Volume ◽  
Before And After ◽  
Functional Defect ◽  
Metabolic Pool ◽  
The Mean

Platelets stored as concentrates (PC) for 72 h at 22 degrees C develop a functional defect. Alterations in adenine nucleotides of platelets have been shown to affect platelet function. Adenine nucleotide content of platelets was measured before and after storage and a decrease of 27.1 /+- 1.7% (mean /+- SE) in ATP and 39.1 /+- 2.6% in ADP were found in 34 PC stored with final volume of 50 ml. In 11 PC with 30 ml volume. ATP and ADP decreased by 39.4 /+- 3.2% and 49.4 /+- 2.1%, respectively. The mean ATP to ADP ratio of stored platelets was significantly higher than of fresh platelets in both groups, suggesting a relatively greater decrease in granular than metabolic pool nucleotides. Levels of low affinity platelet factor 4 measured by radioimmunoassay in plasma from 0.86 /+- 0.08 microgram/ml in the fresh PC to 8.59 /+- 0.39 microgram/ml in stored PC, indicating a concomitant alpha-granular secretion. Labeling of metabolic pool with 14C-adenine revealed a mean decrease in the adenylate energy charge of 2.0 /+- 0.4% in 12 of 16 stored PC, with a lower ATP and higher hypoxanthine labeling in stored as compared to fresh platelets. These observations suggest that stored platelets develop an acquired defect in both dense and alpha granules and in their ability to maintain ATP homeostasis.

Secretion Defect in Platelets Stored at 4°C

1982 ◽  
Vol 47 (03) ◽  
pp. 221-225 ◽  
Author(s):  
A Koneti Rao ◽  
Scott Murphy
Keyword(s):  
Adenine Nucleotides ◽  
Energy Charge ◽  
Total Content ◽  
Adenylate Energy Charge ◽  
Platelet Concentrates ◽  
Functional Changes ◽  
Final Volume ◽  
Metabolic Pool ◽  
The Mean

SummaryTo understand the functional changes induced by storage, we have examined the adenine nucleotides of platelets stored for 72 hr at 22°C and 4°C. Ten platelet concentrates (PC) were stored at each temperature with five in each group having a final volume of 50 ml and 30 ml. The total ATP and ADP content of platelets decreased following storage in all 4 groups of PC, with the decrease being greater in the PC stored at 22°C than those at 4°C. The mean thrombin secretable ATP+ADP content of platelets from PC stored at 22°C and 4°C were 29.7% and 19.7% of the total content, respectively (p <0.001). Thus, cold stored platelets have a higher total content of ATP+ADP but secrete distinctly lesser amounts than 22°C stored platelets. Labeling of the metabolic pool adenylates with 14C-adenine revealed a greater decrease in the adenylate energy charge of the platelets stored at 4°C. The secretion defect demonstrated in cold stored platelets may be related to the inability of these platelets to maintain ATP homeostasis.

scholarly journals Labeling of the releasable adenine nucleotides of washed human platelets

Blood ◽  
1977 ◽  
Vol 49 (1) ◽  
pp. 89-99 ◽  
Author(s):  
HJ Reimers ◽  
MA Packham ◽  
JF Mustard
Keyword(s):  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Human Platelets ◽  
Transport Processes ◽  
Adenylate Energy Charge ◽  
Prolonged Incubation ◽  
Atp Pool ◽  
Adenine Nucleotide Pool

Abstract In rabbit platelets, the metabolically active ATP pool equilibrates with the releasable ATP pool within 1 day. The studies showing this have now been extended to human platelets. Human platelets labeled with 14C-adenosine or 14C-adenine were incubated for up to 10 hr in vitro at 37 degrees C. After 10 hr, about 12% of the total platelet 14C-ATP and 14C-ADP had become releasable with thrombin (4.2 units/ml). Lysis of platelets did not occur, since less than 1% of the platelet-bound 51Cr from platelets labeled with this radioisotope appeared in the ambient fluid upon thrombin treatment. The 14C-ATP/14C-ADP ratio of the released adenine nucleotides (7.6) was similar to the 14C-ATP/14C-ADP ratio of the nonreleasable adenine nucleotides (7.1) 2 hr after the labeling with 14C-adenosine. However, upon prolonged incubation (10 hr) in vitro, the 14C-ATP/14C-ADP ratio of the releasable adenine nucleotides decreased to 2.7. The adenylate energy charge and the 14C- ATP/14C-ADP ratio of the metabolic adenine nucleotide pool did not change significantly during the time of observation. The 14C-ATP content of the platelets decreased by less than 1% hr of incubation at 37 degrees C. These observations are interpreted to mean that the 14C is transferred from the metabolically active, nonreleasable adenine nucleotide pool of human platelets into the releasable adenine nucleotide pool as ATP and is partially hydrolyzed there to yield ADP. The transfer of ATP across the storage organelle membrane of platelets may be similar to transport processes in the chromaffin cells of the adrenal medulla and may represent a general phenomenon in cells that possess storage organelles containing adenine nucleotides.

Changes of platelets’ function in preeclampsia

Open Medicine ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. 696-700
Author(s):  
Goran Babic ◽  
Slobodan Novokmet ◽  
Slobodan Jankovic
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Adenosine Diphosphate ◽  
Control Group ◽  
Adenylate Energy Charge ◽  
Cross Sectional ◽  
Blood Samples ◽  
Metabolic Pool ◽  
Aggregation Of Platelets

AbstractIncreased aggregation of platelets during preeclampsia was shown in several studies, yet several others reported no change. The aim of our study was to investigate platelet aggregation in a group of patients suffering from preeclampsia. In a cross-sectional study blood samples were taken from 89 hospitalized patients in the third trimester of pregnancy: 38 were suffering from mild to moderate preeclampsia and 51 patients were without preeclampsia. From the blood samples platelet aggregation, secretion of adenine nucleotides from platelets, concentration of energy-rich adenine compounds and levels of cyclic adenosine-mono-phosphate and cyclic guanosine mono-phosphate in platelets were measured. In the patients with preeclampsia, the adenosine diphosphate threshold for biphasic aggregation [odds ratio (OR):.75; 95% Confidence Interval (CI): 0.55–1.02; p<0.05], total adenine nucleotides concentration in the metabolic pool of platelets (OR:0.99; CI: 0.62–1.57; p<0.01) and cyclic adenosine-mono-phosphate (OR:0.81; CI: 0.57, 1.14; p<0.05) and cyclic guanosine mono-phosphate (OR:.78; CI: 0.55–1.09; p<0.05) levels in platelets were decreased in comparison with the control group, while adenylate energy charge in the metabolic pool of platelets (OR: >100.00; CI: 0.00->100.00; p<0.05) and secretion of adenosine triphosphate (OR:.13; CI: 0.00–14.26; p<0.05) and adenosine diphosphate (OR:.77; CI: 0.08–36.79; p<0.05) were increased. The results of our study show increased activation and aggregation of platelets in pregnant females with preeclampsia.

AMP deaminase deficiency: Study of the human skeletal muscle purine metabolism during ischaemic isometric exercise

1987 ◽  
Vol 72 (4) ◽  
pp. 475-482 ◽  
Author(s):  
S. P. T. Sinkeler ◽  
R. A. Binkhorst ◽  
E. M. G. Joosten ◽  
R. A. Wevers ◽  
M. M. Coerwinkel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Test ◽  
Adenine Nucleotide ◽  
Energy Charge ◽  
Isometric Exercise ◽  
Creatine Phosphate ◽  
Adenylate Energy Charge ◽  
Amp Deaminase ◽  
Control Subjects ◽  
Before And After

1. Muscle biopsies were taken from 10 control subjects and five AMP deaminase (AMPD) deficient individuals before and after an ischaemic isometric exercise test and analysed for purine nucleotide, NAD+, creatine phosphate (CP) and lactate content. 2. The decrease of ATP induced by the exercise test was significantly lower in the AMPD deficient patients than in the controls, but the decrease of creatine phosphate and the increase of lactate did not differ. There were no significant differences in the exertional performance level between patients and controls and no evidence was obtained of an increased energy expenditure per unit of performance in AMPD deficiency. 3. The AMPD deficient individuals were equally capable of maintaining a high adenylate energy charge (EC) as the control subjects, which indicates a normal regulation of the balance between ATP consumption and ATP regeneration. 4. ATP, ADP and total adenine nucleotide (TAN) but not AMP, were significantly elevated in the AMPD deficient patients as compared with the controls before as well as after the exercise test. This underlines the role of AMPD activity in the adenine nucleotide catabolism of skeletal muscle.

scholarly journals Labeling of the releasable adenine nucleotides of washed human platelets

Blood ◽  
1977 ◽  
Vol 49 (1) ◽  
pp. 89-99 ◽  
Author(s):  
HJ Reimers ◽  
MA Packham ◽  
JF Mustard
Keyword(s):  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Human Platelets ◽  
Transport Processes ◽  
Adenylate Energy Charge ◽  
Prolonged Incubation ◽  
Atp Pool ◽  
Adenine Nucleotide Pool

In rabbit platelets, the metabolically active ATP pool equilibrates with the releasable ATP pool within 1 day. The studies showing this have now been extended to human platelets. Human platelets labeled with 14C-adenosine or 14C-adenine were incubated for up to 10 hr in vitro at 37 degrees C. After 10 hr, about 12% of the total platelet 14C-ATP and 14C-ADP had become releasable with thrombin (4.2 units/ml). Lysis of platelets did not occur, since less than 1% of the platelet-bound 51Cr from platelets labeled with this radioisotope appeared in the ambient fluid upon thrombin treatment. The 14C-ATP/14C-ADP ratio of the released adenine nucleotides (7.6) was similar to the 14C-ATP/14C-ADP ratio of the nonreleasable adenine nucleotides (7.1) 2 hr after the labeling with 14C-adenosine. However, upon prolonged incubation (10 hr) in vitro, the 14C-ATP/14C-ADP ratio of the releasable adenine nucleotides decreased to 2.7. The adenylate energy charge and the 14C- ATP/14C-ADP ratio of the metabolic adenine nucleotide pool did not change significantly during the time of observation. The 14C-ATP content of the platelets decreased by less than 1% hr of incubation at 37 degrees C. These observations are interpreted to mean that the 14C is transferred from the metabolically active, nonreleasable adenine nucleotide pool of human platelets into the releasable adenine nucleotide pool as ATP and is partially hydrolyzed there to yield ADP. The transfer of ATP across the storage organelle membrane of platelets may be similar to transport processes in the chromaffin cells of the adrenal medulla and may represent a general phenomenon in cells that possess storage organelles containing adenine nucleotides.

Hepatic preconditioning preserves energy metabolism during sustained ischemia

2000 ◽  
Vol 279 (1) ◽  
pp. G163-G171 ◽  
Author(s):  
C. Peralta ◽  
R. Bartrons ◽  
L. Riera ◽  
A. Manzano ◽  
C. Xaus ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
High Energy ◽  
Energetic Cost ◽  
Main Role ◽  
Adenylate Energy Charge ◽  
Glycogen Depletion ◽  
Adenine Nucleotide Pool

We evaluated the possibility that ischemic preconditioning could modify hepatic energy metabolism during ischemia. Accordingly, high-energy nucleotides and their degradation products, glycogen and glycolytic intermediates and regulatory metabolites, were compared between preconditioned and nonpreconditioned livers. Preconditioning preserved to a greater extent ATP, adenine nucleotide pool, and adenylate energy charge; the accumulation of adenine nucleosides and bases was much lower in preconditioned livers, thus reflecting slower adenine nucleotide degradation. These effects were associated with a decrease in glycogen depletion and reduced accumulation of hexose 6-phosphates and lactate. 6-Phosphofructo-2-kinase decreased in both groups, reducing the availability of fructose-2,6-bisphosphate. Preconditioning sustained metabolite concentration at higher levels although this was not correlated with an increased glycolytic rate, suggesting that adenine nucleotides and cAMP may play the main role in the modulation of glycolytic pathway. Preconditioning attenuated the rise in cAMP and limited the accumulation of hexose 6-phosphates and lactate, probably by reducing glycogen depletion. Our results suggest the induction of metabolic arrest and/or associated metabolic downregulation as energetic cost-saving mechanisms that could be induced by preconditioning.

Phospholipid and adenine nucleotide metabolism in muscle after burn injury

1985 ◽  
Vol 249 (5) ◽  
pp. R603-R610
Author(s):  
J. Turinsky ◽  
I. H. Chaudry
Keyword(s):  
Burn Injury ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Nucleotide Metabolism ◽  
Adenylate Energy Charge ◽  
Adenine Nucleotide Metabolism ◽  
Limb Muscles ◽  
32P Incorporation

The role of phospholipid and adenine nucleotide metabolism in postburn unresponsiveness of muscle to insulin was examined. A single hindlimb scald in the rat was produced, and 3 days later soleus muscles were incubated in vitro with and without insulin. Under basal conditions muscles from the burned limbs had normal contents of phosphatidylcholine and phosphatidylinositol but decreased diphosphatidylglycerol (-39%) and phosphatidylethanolamine (-24%) and increased sphingomyelin (+62%), lysophosphatidylcholine (+68%), and phosphatidylserine (+13%) compared with the contralateral unburned limb. Such muscle also incorporated 107-396% more [32P]phosphate into all measured phospholipids, except for diphosphatidylglycerol. The presence of insulin had no effect on either the mass of phospholipids or 32P incorporation in any muscle. The burned limb muscles (frozen in situ) also exhibited lower levels of ATP (-25%) and total adenine nucleotides (-24%) than uninjured muscle but normal adenylate energy charge. The burned limb muscles had lower adenosine (-37%), but inosine and hypoxanthine were 82 and 39% higher, respectively. These data suggest recovery of muscle from local thermal injury is associated with alterations in mass, and possibly also turnover, of tissue phospholipids, the measured phospholipids do not mediate the postreceptor action of insulin in normal muscle, energy charge of the recovering injured muscle is restored before ATP level at the time when this muscle is unresponsive to insulin stimulation.

scholarly journals Energy Requirement for Maintenance of Adenylate Energy Charge and Metabolic ATP in Platelets During Starvation

1977 ◽  
Author(s):  
J.W.N. Akkerman ◽  
G. Gorter ◽  
J.J. Sixma
Keyword(s):  
Steady State ◽  
Adenine Nucleotides ◽  
Energy Requirement ◽  
Energy Charge ◽  
Lactate Production ◽  
Stable Steady State ◽  
Adenylate Energy Charge ◽  
Consumption Energy ◽  
Steady State Levels ◽  
Lactate Formation

Energy requirements for maintenance of stable adenylate energy charge (AEC) and metabolic ATP(ATP-m)level were studied in gel filtered platelets at various degrees of starvation. Platelets gel filtered and subsequently incubated during 40 min.at 37°C with 1mM CN- and without glucose consumed their glycogen at a rate of 0.79 ± 0.23(± SD, n=6)/μmol glycosyl residues .min-1 10-11 cells. During this period AEC and ATP-m decreased linearly with time at rates of 5-6.10-3 and 0.75-1.05% of total radioactive adenine nucleotides .min-1.10-11 cells respectively. Addition of 25–1000μM glucose increased lactate production and decreased the fall of AEC and ATP-m proportional to the amounts of glucose added. Glycogenolysis remained active below 100μM glucose but ceased at higher glucose concentrations. From these data ATP-m production from glycogenolysis and glycolysis was calculated and compared with the decrease of steady state levels of AEC and ATP-m. A production of 3μmol ATP-m.min-1.10-11 cells was required to maintain initial AEC and ATP-m level. At lower rates of ATP-m production these values fell without reaching stable steady state levels in a lower range. After 40-50 min variations in AEC and ATP-m ceased and lactate formation stopped leaving the cells in a state of hybernation. Subsequent addition of glucoserestored lactate accumulation, AEC and ATP-m. On the basis of formation and steady state levels of ATP-m its consumption was calculated. A lowering production was not completely met by a lowering consumption. Energy consumption in resting platelets is therefore partly independent from energy production.

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