scholarly journals Studies on the mechanism of ristocetin-induced platelet aggregation

Blood ◽  
1975 ◽  
Vol 45 (1) ◽  
pp. 91-96 ◽  
Author(s):  
HE Kattlove ◽  
MH Gomez
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Platelet Membranes ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

Abstract Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.

scholarly journals Studies on the mechanism of ristocetin-induced platelet aggregation

Blood ◽  
1975 ◽  
Vol 45 (1) ◽  
pp. 91-96
Author(s):  
HE Kattlove ◽  
MH Gomez
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Platelet Membranes ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.

scholarly journals The Effect of Cold on Platelets. III. Adenine Nucleotide Metabolism After Brief Storage at Cold Temperature

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 557-564 ◽  
Author(s):  
Herman E. Kattlove ◽  
Dorothy Mormino
Keyword(s):  
Connective Tissue ◽  
Prostaglandin E1 ◽  
Room Temperature ◽  
Adenine Nucleotide ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Nucleotide Metabolism ◽  
Immunoglobulin M ◽  
Release Reaction ◽  
Adenine Nucleotide Metabolism

Abstract The effect of cold on platelet adenine nucleotide (PAN) metabolism was studied. Spontaneous aggregation which occurs when chilled platelet-rich plasma (PRP) is simultaneously warmed and stirred was not accompanied by the changes in adenine nucleotides associated with the release reaction. Connective tissue caused the release of the same amount of ADP and conversion of equal amounts of ATP to IMP and hypoxanthine in cold-stored platelets as it did in room temperature stored platelets. However, cold did have an important effect on PAN. In PRP stored at cold (0° C, 3° C) temperatures and warmed up to 37° C in the presence of 3H adenine, there was an increase in the conversion of adenine to its metabolites and ultimately to hypoxanthine as compared to PRP stored at warmer temperatures. This effect could not be prevented by ouabain, prostaglandin E1, antibody to immunoglobulin M or adenosine.

scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

Adenine Nucleotide Metabolism of Human Platelets during Collagen-Induced Aggregation

1972 ◽  
Vol 27 (03) ◽  
pp. 416-424
Author(s):  
M Murakami ◽  
K Yoshino ◽  
M Takase ◽  
K Odake
Keyword(s):  
Light Transmission ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Rapid Change ◽  
Human Platelets ◽  
Nucleotide Metabolism ◽  
Intracellular Atp ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

SummaryChanges in platelet adenine nucleotides during collagen-induced aggregation were estimated. Averaged values of ATP and ADP in intact platelets were 56.3 and 28.9 attomoles per platelet, respectively. After collagen-induced aggregation, intracellular ATP plus ADP was depleted to about half of that in intact platelets. The released ADP accounted for 13% of that in intact platelets.Behavior of platelet adenine nucleotides during aggregation was divided into the following phases. At first, platelet ATP decreased without the release of nucleotides. The release of ADP occurred at the stage of rapid change of light transmission. Subsequently, the released ADP decomposed in parallel with the degradation of intracellular ADP. The radioactive ATP in platelets decreased during exposure to collagen, without appreciable release of radioactive nucleotides. The ATP released from disrupted platelets was rapidly metabolized in plasma.

scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756 ◽  
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

Abstract The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

Oxidative phosphorylation, adenine nucleotides, and phosphofructokinase in the livers of rats receiving thrombogenic diets

1969 ◽  
Vol 47 (1) ◽  
pp. 39-46
Author(s):  
Nicole Simard-Duquesne
Keyword(s):  
Platelet Aggregation ◽  
Oxidative Phosphorylation ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Nucleotide Metabolism ◽  
Standard Laboratory ◽  
Relation Directe ◽  
Adenine Nucleotide Metabolism ◽  
Phosphofructokinase Activity ◽  
Nucleotide Ratio

Diets of varying thrombogenic potencies were fed to rats for a period of 6 weeks. The thrombogenic potency of these diets was determined by the extent of the hepatic infarcts (consequent upon thrombosis in the hepatic vein) which occurred within 24 h after the injection of S. typhosa endotoxin. Those groups of rats receiving the low thrombogenic diets were more suitable as controls for the animals on the high thrombogenic diets than were normal rats fed standard laboratory chow. The thrombogenic potency of the diets was inversely related to the ratio of [AMP][ATP]/[ADP]2 found in the liver. A decrease in this ratio should favor platelet aggregation, and the results are thus in accord with the hypotheses implicating adenine nucleotides in thrombogenesis. The thrombogenic potency of the diets was directly related to the activity of liver phosphofructokinase. This increase in activity is probably linked to the disturbed adenine nucleotide metabolism. Oxidative phosphorylation mechanisms were investigated as possible causes for the changes in adenine nucleotides, but no important alteration in these reactions could be demonstrated. The exact mechanism by which the thrombogenic diets alter the adenine nucleotide ratio and the phosphofructokinase activity remains to be elucidated.Des rats ont été nourris pendant 6 semaines avec des régimes de forces thrombogènes variées. Cette capacité thrombogène est évaluée d'après la sévérité des infarcti hépatiques (provoqués par un thrombus dans la veine hépatique) que l'on trouve en dedans de 24 h après l'injection d'endotoxine de S. typhosa. Les groupes de rats sur régimes thrombogènes à force faible constituent de meilleurs groupes témoins que ne le sont des animaux, recevant un régime usuel. La force thrombogène de ces régimes est en relation inverse avec le rapport [AMP][ATP]/[ADP]2 que l'on trouve dans le foie. Un abaissement de ce rapport devrait favoriser l'agrégation des plaquettes sanguines; les résultats obtenus supportent les hypothèses selon lesquelles les nucléotides d'adénine sont impliqués dans la thrombogénèse. L'activité de la phosphofructokinase est augmentée en relation directe avec la force thrombogène des régimes. Cette augmentation est probablement liée au métabolisme anormal des nucleotides d'adénine. Aucun changement n'a pu être décelé dans les mécanismes de phosphorylation oxydative, qui pourraient provoquer des altérations dans le métabolisme des nucléotides d'adénine. Le mécanisme exact par lequel les régimes thrombogènes agissent au niveau des nucléotides d'adénine et de la phosphofructokinase est inexpliqué.

The Platelet of the Newborn Infant – Adenine Nucleotide Metabolism and Release

1980 ◽  
Vol 43 (02) ◽  
pp. 099-103 ◽  
Author(s):  
J M Whaun ◽  
P Lievaart ◽  
Keyword(s):  
Newborn Infant ◽  
Adenine Nucleotide ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Newborn Infants ◽  
Specific Radioactivity ◽  
Nucleotide Metabolism ◽  
Breakdown Product ◽  
Term Infants ◽  
Adenine Nucleotide Metabolism

SummaryBlood from normal full term infants, mothers and normal adults was collected in citrate. Citrated platelet-rich plasma was prelabelled with 3H-adenine and reacted with release inducers, collagen and adrenaline. Adenine nucleotide metabolism, total adenine nucleotide levels and changes in sizes of these pools were determined in platelets from these three groups of subjects.At rest, the platelet of the newborn infant, compared to that of the mother and normal adult, possessed similar amounts of adenosine triphosphate (ATP), 4.6 ± 0.2 (SD), 5.0 ± 1.1, 4.9 ± 0.6 µmoles ATP/1011 platelets respectively, and adenosine diphosphate (ADP), 2.4 ± 0.7, 2.8 ± 0.6, 3.0 ± 0.3 umoles ADP/1011 platelets respectively. However the marked elevation of specific radioactivity of ADP and ATP in these resting platelets indicated the platelet of the neonate has decreased adenine nucleotide stores.In addition to these decreased stores of adenine nucleotides, infant platelets showed significantly impaired release of ADP and ATP on exposure to collagen. The release of ADP in infants, mothers, and other adults was 0.9 ± 0.5 (SD), 1.5 ± 0.5, 1.5 ± 0.1 umoles/1011 platelets respectively; that of ATP was 0.6 ± 0.3, 1.0 ± 0.1,1.3 ± 0.2 µmoles/1011 platelets respectively. With collagen-induced release, platelets of newborn infants compared to those of other subjects showed only slight increased specific radioactivities of adenine nucleotides over basal levels. The content of metabolic hypoxanthine, a breakdown product of adenine nucleotides, increased in both platelets and plasma in all subjects studied.In contrast, with adrenaline as release inducer, the platelets of the newborn infant showed no adenine nucleotide release, no change in total ATP and level of radioactive hypoxanthine, and minimal change in total ADP. The reason for this decreased adrenaline reactivity of infant platelets compared to reactivity of adult platelets is unknown.Infant platelets may have different membranes, with resulting differences in regulation of cellular processes, or alternatively, may be refractory to catecholamines because of elevated levels of circulating catecholamines in the newborn period.

Sign in / Sign up

Export Citation Format

Share Document