Platelet volume and intraplatelet adenine nucleotides in various hematologic disorders

2009 ◽  
Vol 40 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Hiroyuki Nozaki ◽  
Tadami Nagao ◽  
Shigeru Arimori
Keyword(s):  
Adenine Nucleotides ◽  
Platelet Volume ◽  
Hematologic Disorders

Decrease in Platelet Adenine Nucleotides Content In Patients With Dic, Thrombosis and After Operation

1979 ◽  
Author(s):  
H. Yamazaki ◽  
T. Motomiya ◽  
N. Miyagawa ◽  
C. Watanabe ◽  
Y. Yahara ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Time Course ◽  
Adenine Nucleotides ◽  
Firefly Luciferase ◽  
Acute Stage ◽  
Platelet Volume ◽  
Recovery Stage ◽  
Release Reaction ◽  
Postoperative State

Conditions which induce platelet release reaction in vivo are not yet obvious. To detect the conditions, platelet ATP and ADP content (firefly luciferase method) and plasma beta-thromboglobulin level were measured in 51 healthy young volunteers, 10 patients with typical DIC syndrome during time course of cancer, 27 patients in acute stage of thrombosis in cerebral, coronary and femoral arteries, 29 patients in recovery stage of thrombosis and 69 patients one day before, and one day, one week and one month after a laparotomy. Platelet count and volume were counted by a Coulter Counter and Channelyzer. Platelet aggregation induced by ADP, adrenaline and collagen was also measured. In the healthy, platelet mode volume was 4.21 ± 0.08 μ3 (mean ± SE). beta-TG was 29.9 ± 5.9 ng/ml, and ATP and ADP contents were 5.81 ± 0.17 and 3.19 ± 0.09 μmoles/1011 platelets and ATP/ADP was 1.82 ± 0.05. In DIC, acute stage of thrombosis and one week after laparotomy, platelet volume became to smaller and ADP content decreased significantly. Changes in beta-TG level were rather variable. Platelet aggregation increased in thrombosis and postoperative state, while it decreased in DIC. In DIC, decrease in ATP and ADP content was marked as compared with other groups. It suggests that ADP content In platelets may reflect release reaction in vivo. Following the release reaction, platelet aggregability may increase. However, platelets with large decrease in adenine nucleotides content may have hypofunction.

Klinische und labordiagnostische Parameter bei 21 Hunden mit primärer immunvermittelter Thrombozytopenie

2011 ◽  
Vol 39 (01) ◽  
pp. 17-24 ◽  
Author(s):  
H. J. Schuberth ◽  
R. Mischke ◽  
B. Dircks
Keyword(s):  
Mean Platelet Volume ◽  
Platelet Volume ◽  
Klinische Relevanz

Zusammenfassung Gegenstand und Ziel: Charakterisierung von klinischen und labordiagnostischen Parametern sowie Therapie und Krankheitsverlauf bei Hunden mit einer angenommenen primären immunvermittelten Thrombozytopenie (pIMT) und Identifizierung möglicher Besonderheiten im Vergleich zu Hunden mit einer sekundären immunvermittelten Thrombozytopenie (sIMT). Material und Methoden: Retrospektive Auswertung von Patientendaten thrombozytopenischer Hunde, bei denen plättchengebundene Antikörper mittels Durchflusszytometrie nachgewiesen wurden. Ergebnisse: Dreizehn der 21 Hunde (62%) mit einer pIMT waren männlich. Das mittlere Alter bei Erstvorstellung betrug 6,6 Jahre (1,6–13,5 Jahre [Median; Minimum–Maximum]). Blutungen, hauptsächlich in Form von Haut- und Schleimhautblutungen, lagen bei 18 Hunden (86%) vor. Neunzehn Hunde (91%) wiesen eine Thrombozytenzahl unter 20000/μl auf. Bei allen Hunden mit einer pIMT ergab sich ein mittleres Thrombozytenvolumen (mean platelet volume, MPV) im oder unter dem Referenzbereich. In nahezu allen Fällen bestand eine gesteigerte Megakaryopoeseaktivität. Der Vergleich zweier Therapieregime (Prednisolon versus Prednisolon und Azathioprin) zeigte keinen signifikanten Unterschied bezüglich der Zeit bis zum Erreichen einer Thrombozytenzahl im Referenzbereich. Zwischen Patienten mit pIMT oder sIMT ließ sich im Hinblick auf Alter und Geschlecht kein signifikanter Unterschied feststellen. Bei Hunden mit einer pIMT waren Thrombozytenzahl und MPV signifikant niedriger und die Megakaryopoeseaktivität signifikant häufiger erhöht. Schlussfolgerung und klinische Relevanz: Bei Hunden, die plättchengebundene Antikörper und zusätzlich eine schwere Thrombozytopenie, ein niedriges MPV und eine gesteigerte Megakaryopoeseaktivität aufweisen, ist eine pIMT naheliegend.

The Action Mechanism of the Purified Platelet Aggregation Principle of Trimeresurus mucrosquamatus Venom

1979 ◽  
Vol 41 (03) ◽  
pp. 475-490 ◽  
Author(s):  
Chaoho Ouyang ◽  
Che-Ming Teng
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotides ◽  
Muscle Relaxants ◽  
Prostaglandin Synthesis ◽  
Action Mechanism ◽  
Crude Venom ◽  
Platelet Factor ◽  
Induce Platelet Aggregation ◽  
Minimal Concentration ◽  
Aggregation Principle

SummaryThe minimal concentration of the platelet aggregation principle (Platelet Aggregoserpen- tin, PAS) necessary to induce platelet aggregation was 10 ng/ml, about one-hundredth of that of the crude venom. PAS induced the release of platelet factors 3 and 4 from platelets, but the released platelet factor 3 was easily inactivated by the anti-phospholipid effect of PAS. Pretreatment of platelets with neuraminidase potentiated PAS-induced platelet aggregation. PAS-induced platelet aggregation was independent on released ADP; it could occur in the ADP-removing systems, such as apyrase or a combination of phosphoenolpyruvate and pyruvate kinase. However, PAS-induced platelet aggregation could be inhibited by adenine nucleotides and adenosine.PAS-induced platelet aggregation was inhibited by some anti-inflammatory agents, antimalarial drugs, local anesthetics, antihistamine and smooth muscle relaxants. After deaggregation of PAS-treated platelets, thrombin and sodium arachidonate could further induce platelet aggregation, but ADP and second dose of PAS could not. It is concluded that PAS-induced platelet aggregation is due to prostaglandin synthesis. Recent literatures on the mechanism of platelet aggregation were surveyed and the actions of PAS were discussed.

Acute and Chronic Changes in Platelet Volume and Count After Cardiopulmonary Bypass Induced Thrombocytopenia in Man

1987 ◽  
Vol 57 (01) ◽  
pp. 55-58 ◽  
Author(s):  
J F Martin ◽  
T D Daniel ◽  
E A Trowbridge
Keyword(s):  
Platelet Count ◽  
Mean Platelet Volume ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Control Group ◽  
Artery Bypass Graft ◽  
Platelet Volume ◽  
Young Males ◽  
The Mean

SummaryPatients undergoing surgery for coronary artery bypass graft or heart valve replacement had their platelet count and mean volume measured pre-operatively, immediately post-operatively and serially for up to 48 days after the surgical procedure. The mean pre-operative platelet count of 1.95 ± 0.11 × 1011/1 (n = 26) fell significantly to 1.35 ± 0.09 × 1011/1 immediately post-operatively (p <0.001) (n = 22), without a significant alteration in the mean platelet volume. The average platelet count rose to a maximum of 5.07 ± 0.66 × 1011/1 between days 14 and 17 after surgery while the average mean platelet volume fell from preparative and post-operative values of 7.25 ± 0.14 and 7.20 ± 0.14 fl respectively to a minimum of 6.16 ± 0.16 fl by day 20. Seven patients were followed for 32 days or longer after the operation. By this time they had achieved steady state thrombopoiesis and their average platelet count was 2.44 ± 0.33 × 1011/1, significantly higher than the pre-operative value (p <0.05), while their average mean platelet volume was 6.63 ± 0.21 fl, significantly lower than before surgery (p <0.001). The pre-operative values for the platelet volume and counts of these patients were significantly different from a control group of 32 young males, while the chronic post-operative values were not. These long term changes in platelet volume and count may reflect changes in the thrombopoietic control system secondary to the corrective surgery.

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.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

Newborn Platelet Dysfunction: a Storage Pool and Release Defect

1976 ◽  
Vol 36 (01) ◽  
pp. 200-207 ◽  
Author(s):  
Donald G. Corby ◽  
Thomas F. Zuck
Keyword(s):  
Specific Activity ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Blood Platelets ◽  
Newborn Infants ◽  
Specific Radioactivity ◽  
High Dose ◽  
Platelet Dysfunction ◽  
Paired Samples ◽  
Normal Adults

SummaryPer cent aggregation, release and content of adenine nucleotides, and specific radioactivity were evaluated in citrated platelet-rich plasma (PRP) prepared from paired samples of maternal and cord blood. Platelets of newborn infants aggregated normally in response to high dose ADP (20 μM), strong collagen suspensions, and thrombin; however, when compared with PRP from the mothers or from normal adults, per cent aggregation in response to lower concentrations of ADP (2 μM), weak collagen, and part particularly epinephrine was markedly reduced. Nucleotide release after stimulation of the newborns’ PRP with the latter two inducers was also impaired. ATP and ADP content of the newborns’ platelets was also significantly less than that of their mothers or of normal adults, but specific activity was normal. The data suggest that the impairment of ADP release in the platelets of newborn infants is due to decreased sensitivity to external stimuli. Since metabolic ATP is necessary for the platelet release reaction, it is postulated that the platelet dysfunction results from a lack of metabolic ATP.

A Relationship between Platelet Volume and Platelet Number

1974 ◽  
Vol 31 (02) ◽  
pp. 363-365 ◽  
Author(s):  
J. R O’Brien ◽  
Sandra Jamieson
Keyword(s):  
Platelet Volume ◽  
Platelet Number

Physiological Effects of Nonimmune Platelet Associated Immunoglobulin G

1981 ◽  
Vol 45 (01) ◽  
pp. 027-033 ◽  
Author(s):  
K Sugiura ◽  
M Steiner ◽  
M Baldini
Keyword(s):  
Shape Change ◽  
Fluorescein Isothiocyanate ◽  
Recovery Phase ◽  
Human Platelets ◽  
Serotonin Release ◽  
Platelet Volume ◽  
Igg Antibody ◽  
Heterologous Antiserum ◽  
Igg Binding ◽  
Series Of Experiments

SummaryThe function of nonimmune IgG associated with platelets is unknown. In a series of experiments we have investigated this problem, relating amount of platelet-associated IgG (PAIgG) to platelet volume, serotonin release, adherence of platelets to monocytes and platelet senescence. Most of these studies were performed with human platelets. Platelets freed of preexisting PAIgG by incubation at 22° C were incubated with IgG in a series of concentrations ranging from 0.4 — 27.0 X10-6 M. The IgG preparations used were demonstrably free of aggregated forms of the protein. The amount of PAIgG bound to platelets was determined by the use of fluorescein isothiocyanate-conjugated anti-IgG antibody (F-anti-IgG antibody) which was quantified in a fluorospectrophotometer. Newly bound IgG was assayed similarly by the use of F-IgG. A dose-dependent increase in platelet volume was associated with the binding of nonimmune IgG by platelets. The process which leveled off at an IgG concentration of 1.2 —1.5 X10-5 M was almost fully reversible and was not due to platelet shape change or aggregation. Release of serotonin from IgG-treated platelets was relatively small but to the extent that it occurred was positively related to the IgG concentration to which platelets were exposed. Adherence to autologous monocytes studied quantitatively by the use of formaldehyde-fixed cells was also positively related to the amount of IgG on the platelets. Normal or IgG-defident serum had a potent inhibitory (noncompetitive) action on the binding of F-IgG and F-anti-human IgG antibody to human platelets. Cohorts of platelets prepared in rabbits during the recovery phase of immunological thrombocytopenia induced by injection of heterologous antiserum, showed an age-dependent increase of PAIgG and of IgG binding. These results suggest that PAIgG plays a role in the clearance of senescent platelets.

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