Microparticle counts in platelet-rich and platelet-free plasma, effect of centrifugation and sample-processing protocols

2012 ◽  
pp. 1 ◽  
Author(s):  
Wayne L. Chandler
Keyword(s):  
Sample Processing ◽  
Free Plasma ◽  
Plasma Effect

Studies on the Thromboplastic Effect of Human Plasma Lipoproteins

1976 ◽  
Vol 35 (01) ◽  
pp. 178-185 ◽  
Author(s):  
Helena Sandberg ◽  
Lars-Olov Andersson
Keyword(s):  
High Density Lipoprotein ◽  
Human Plasma ◽  
Platelet Rich Plasma ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Free Plasma ◽  
Good Agreement

SummaryHuman plasma lipoprotein fractions were prepared by flotation in the ultracentrifuge. Addition of these fractions to platelet-rich, platelet-poor and platelet-free plasma affected the partial thromboplastin and Stypven clotting times to various degrees. Addition of high density lipoprotein (HDL) to platelet-poor and platelet-free plasma shortened both the partial thromboplastin and the Stypven time, whereas addition of low density lipoprotein and very low density lipoprotein (LDL + VLDL) fractions only shortened the Stypven time. The additions had little or no effect in platelet-rich plasma.Experiments involving the addition of anti-HDL antibodies to plasmas with different platelet contents and measuring of clotting times produced results that were in good agreement with those noted when lipoprotein was added. The relation between structure and the clot-promoting activity of various phospholipid components is discussed.

Stability of Prostacyclin in Human Plasma and Whole Blood: Studies on the Protective Effect of Albumin

1981 ◽  
Vol 46 (03) ◽  
pp. 645-647 ◽  
Author(s):  
M A Orchard ◽  
C Robinson
Keyword(s):  
Platelet Aggregation ◽  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Protective Effect ◽  
Whole Blood ◽  
Bovine Serum ◽  
Fatty Acid Content ◽  
Krebs Solution ◽  
Antiaggregatory Activity ◽  
Free Plasma

SummaryThe biological half-life of prostacyclin in Krebs solution, human cell-free plasma or whole blood was measured by bracket assay on ADP-induced platelet aggregation. At 37°C, pH 7.4, plasma and blood reduced the rate of loss of antiaggregatory activity compared with Krebs solution. The protective effect of plasma was greater than that of whole blood. This effect could be partially mimicked by the addition of human or bovine serum albumin to the Krebs solution. The stabilisation afforded by human serum albumin was dependent on the fatty acid content of the albumin, although this was less important for bovine serum albumin.

The Influence of Serotonin on Clot Retraction and the Thrombelastogram

1958 ◽  
Vol 02 (01/02) ◽  
pp. 111-124 ◽  
Author(s):  
E Deutsch ◽  
K Martiny
Keyword(s):  
Human Plasma ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Specific Effect ◽  
High Dose ◽  
Clot Retraction ◽  
Platelet Counts ◽  
Essential Value ◽  
High Doses ◽  
Free Plasma

Summary1. Normal platelets are necessary for induction of normal clot retraction.2. Serotonin does not induce retraction in human platelet-free plasma-clots or enhance clot firmness as measured in the coagulogram.3. Serotonin does not improve clot retraction or firmness in plasma clots with sub-optimal platelet counts.4. Methylserotonin inhibits clot retraction of platelet-rich plasma to a certain extent in moderate doses, whereas, high doses are ineffective. BOL 148 has a similar, but less significant action. There is a possibility that these effects are specific antiserotonin-effects.5. LSD 25 was ineffective in all concentrations used.6. Largactil and reserpin inhibit retraction in high doses. There seems to be a non specific effect caused by the high dose.7. Reserpine does not release a retraction-inducing agent from the platelets, which could be detected in the centrifuged platelet-free plasma used for the incubation.8. Serotonin does not replace the retraction-cofactor of Hartert, or the dialyzable factor of Lüscher in synthetic clotting substrates.9. Serotonin is of no essential value in inducing normal retraction of human plasma clots.

LEVELS OF FREE PLASMA AMINO ACIDS UNDER ACUTE NORMOBARIC HYPOXIA IN VOLUNTEERS IN FASTED AND POSTPRANDIAL STATES

2020 ◽  
pp. 108-117
Author(s):  
A.A. Chernykh ◽  
N.N. Potolitsyna ◽  
E.A. Burykh ◽  
E.R. Boyko
Keyword(s):  
Amino Acids ◽  
Normobaric Hypoxia ◽  
Adaptation To Hypoxia ◽  
Plasma Amino Acids ◽  
Fed State ◽  
Metabolic Substrates ◽  
Overnight Fasting ◽  
Group 2 ◽  
Free Plasma ◽  
Group 1

The aim of the study was to assess the effect of acute normobaric hypoxia on free plasma amino acids (AA) in volunteers after overnight fasting and in the fed state. Materials and Methods. Group 1 (n=13, aged 22–32) participated in the study in the morning after overnight fasting. Group 2 (n=9, aged 22–32) took part in the study after a light fat-free breakfast. Acute normobaric hypoxia was achieved by breathing a hypoxic gas mixture (9 % O2 and 91 % N2) through a mask. According to the experimental protocol, blood sampling from the cubital vein was performed for analysis. Free plasma amino acids were analyzed using the Aracus amino acid analyzer. Results. Prior to the hypoxia onset, at the 5th and 20th minutes of hypoxia, no statistically significant differences in free AA levels were observed in the groups (p>0.05). At the 10th minute of hypoxia the levels of four AAs (serine, threonine, glutamine, and histidine) were significantly higher in Group 1 than in Group 2 (p<0.05). This was probably due to differences in functioning of several key “harmonizing” AA transporters (ASCT1 (SLC1A4), ASCT2 (SLC1A5) and LAT1 (SC7A5)), for which the AAs were metabolic substrates. It can be assumed, that such changes were caused by currently unclear mechanisms of fast regulation of AA transporter activity, associated with nutritional status. Conclusion. We believe that our findings may be important for providing better adaptation to hypoxia, and for more efficient correction of hypoxic negative effects. Keywords: acute normobaric hypoxia, free plasma amino acids, human. Цель исследования: изучить воздействие острой нормобарической гипоксии на метаболизм свободных аминокислот (АК) плазмы крови у добровольцев, участвовавших в исследовании натощак и после лёгкого завтрака. Материалы и методы. Первая группа добровольцев (22–32 года, n=13) участвовала в исследовании утром натощак, вторая группа (22–32 года, n=9) – через 2–3 ч после лёгкого безжирового завтрака. Гипоксия создавалась путём подачи через маску дыхательной смеси, содержащей 9 % О2 и 91 % N2. В соответствии с протоколом проводился периодический забор крови из локтевой вены для анализа. Оценка уровней свободных АК плазмы крови производилась с помощью аминокислотного анализатора Aracus. Результаты. До начала гипоксии, на 5-й и 20-й мин гипоксии уровни свободных АК в первой и второй группах значимо не различались (p>0,05). На 10-й мин гипоксии между первой и второй группами наблюдались статистически значимые различия уровней четырёх АК: глутамина, серина, треонина и гистидина (p<0,05). Это, вероятно, было обусловлено изменениями в работе «гармонизирующих» мембранных транспортёров (ASCT1 (SLC1A4), ASCT2 (SLC1A5) и LAT1 (SC7A5)), для которых эти АК являются обменными субстратами. Можно предположить, что данные изменения были опосредованы пока неясными механизмами быстрой регуляции активности этих транспортёров, зависящими от питания. Выводы. Мы полагаем, что полученные результаты могут иметь значение для обеспечения адаптации организма человека к острой гипоксии и эффективной коррекции последствий гипоксического воздействия. Ключевые слова: острая нормобарическая гипоксия, свободные аминокислоты плазмы крови, человек.

Sign in / Sign up

Export Citation Format

Share Document