scholarly journals Changes in the functional state of platelets in patients with polytrauma

2021 ◽  
Vol 17 (1) ◽  
pp. 27-32
Author(s):  
M.B. Vyshynska
Keyword(s):  
Platelet Activation ◽  
Blood Clotting ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Platelet ◽  
Normal Number ◽  
Platelet Thrombus ◽  
Primary Activation ◽  
Primary Platelet

Background. Polytrauma remains the leading cause of global morbidity and mortality and is the cause of more than 10 % of deaths. The purpose of this research was to study the lite­rature data about changes in vascular platelet hemostasis, to investigate the dynamics of the morphofunctional state of platelets, to analyze changes in intravascular platelet activation in patients with polytrauma. Results. Normal blood clotting requires at least 4 components — blood vessels, platelets, the ability of blood to coagulate and fibrinolysis. Determination of components such as indicators of intravascular platelet activation can be an important step in assessing disorders of platelet hemostasis in patients with polytrauma. Vascular platelet hemostasis begins with primary reflex spasm of arterioles, followed by secondary spasm of arterioles, then primary platelet plug is formed (adhesion and aggregation), and, accor­dingly, the consolidation of the thrombus, resulting in the formation of the final platelet thrombus. Even before the contact of platelets with naked collagen, the primary activation of platelets occurs. Initially, the shape of intact platelets changes from discoid form to activated cells of discoechinocytes, spherocytes and, or, spheroechinocytes. We found that on day 3 after injury, with a normal number of platelets in the venous blood, the number of intact platelets, discocytes, decreases, the number of active forms of thrombocytes, discoechinocytes and spheroechinocytes, increases, and, accor­dingly, the total amount of active forms of thrombocytes increases. Normal platelet counts in patients with polytrauma may mask the severity of coagulopathy, and studies of intravascular platelet activation may be a diagnostic component of the vascular platelet hemostasis in patients with polytrauma. Conclusions. In patients with coagulopathy due to polytrauma, there are changes in intravascular platelet activation and platelet aggregation, induced by adrenaline and adenosine diphosphate, on day 3.

Assessment of the incorporation of revascularized fibula grafts used for mandibular reconstruction with F-18-PET

2001 ◽  
Vol 40 (02) ◽  
pp. 51-58 ◽  
Author(s):  
H. Schliephake ◽  
van den Hoff ◽  
W. H. Knapp ◽  
G. Berding
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Venous Blood ◽  
Mandibular Reconstruction ◽  
Reference Region ◽  
Osteoblastic Activity ◽  
Non Union ◽  
Range Of Values ◽  
Measured Input

Summary Aim: Determination of the range of regional blood flow and fluoride influx during normal incorporation of revascularized fibula grafts used for mandibular reconstruction. Evaluation, if healing complications are preceded by typical deviations of these parameters from the normal range. Assessment of the potential influence of using “scaled population-derived” instead of “individually measured” input functions in quantitative analysis. Methods: Dynamic F-l 8-PET images and arterialized venous blood samples were obtained in 11 patients early and late after surgery. Based on kinetic modeling regional blood flow (K1) and fluoride influx (Kmlf) were determined. Results: In uncomplicated cases, early postoperative graft K1 - but not Kmlf -exceeded that of vertebrae as reference region. Kmn values obtained in graft necrosis (n = 2) were below the ranges of values observed in uncomplicated healing (0.01 13-0.0745 ml/min/ml) as well as that of the reference region (0.0154-0.0748). Knf values in mobile non-union were in the lower range - and those in rigid non-union in the upper range of values obtained in stable union (0.021 1-0.0694). If scaled population-derived instead of measured input functions were used for quantification, mean deviations of 23 ± 17% in K1 and 12 ± 16% in Kmlf were observed. Conclusions: Normal healing of predominantly cortical bone transplants is characterized by relatively low osteoblastic activity together with increased perfusion. It may be anticipated that transplant necrosis can be identified by showing markedly reduced F− influx. In case that measured input functions are not available, quantification with scaled population-derived input functions is appropriate if expected differences in quantitative parameters exceed 70%.

A 3.5-Second Phenomenon in Haemostasis

1973 ◽  
Vol 30 (02) ◽  
pp. 363-370
Author(s):  
D Thilo ◽  
E Böhm
Keyword(s):  
Bleeding Time ◽  
Rat Skin ◽  
Fibrin Formation ◽  
Bleeding Area ◽  
Platelet Thrombus ◽  
Platelet Aggregates ◽  
Primary Platelet ◽  
System Mechanism

SummaryExperiments with injury of the abdominal rat skin were carried out to examine the haemostatic system mechanism in vivo after zero to 30 seconds bleeding time. In the bleeding area only a few platelet aggregates could be found with no primary platelet thrombus. After 3.5 second bleeding time the first fibrin strands have been observed at the site of injury. The hypothesis is put forward that there is a very fast reacting haemostatic mechanism which results in the fibrin formation already at 3.5 seconds.

On The Mechanism Of Heparin-Induced Potentiation Of Platelet Aggregation

1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Coagulation Factors ◽  
Marked Enhancement ◽  
Matrix Bound ◽  
Induced Aggregation ◽  
Aggregation Of Platelets ◽  
Plasma Heparin

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.

Human Prothrombin Activation: Determination of Plasma and Serum Levels of Prothrombin Fragment 3 by Radioimmunoassay

1979 ◽  
Author(s):  
Daniel Walz ◽  
Thomas Brown
Keyword(s):  
Blood Clotting ◽  
Factor Xa ◽  
Heart Association ◽  
Serum Levels ◽  
Cross Reactivity ◽  
Assay Procedure ◽  
A Chain ◽  
Prothrombin Activation ◽  
Theoretical Amount

Human prothrombin activation is unique in that, in addition to the release of fragment 1.2 (FI.2) from the NH-terminus of prothrombin by factor Xa during the generation of thrombin, an additional 13 residue polypeptide, fragment 3 (F3), is autocatalytically removed from the amino-terminus of the thrombin A chain. We have developed a rapid radioimmunoassay for human F3 which incorporates short incubation times and the use of a preprecipitated second antibody; the assay can be performed in three hours. Specificity studies in buffer systems show prothrombin and prethrombin 1 cross-reacting at a level of 0.001; purified thrombin does not cross-react. In the presence of 5% BSA, prothrombin displays considerably less cross-reactivity. No immunoreactive material to F3 antibodies could be detected in 400 μL of plasma. Serum, obtained from whole blood clotting, contained measurable quantities of F3 (40-100 ng/mL). This amount in serum represents only 5-10% of the theoretical amount available should all of the fragment be hydrolytically cleaved during the conversion of prothrombin to thrombin. This assay procedure is currently being utilized to monitor the activation of purified human prothrombin in the absence and presence of selected plasma inhibitors. (Supported in part by NIH 05384-17 and the Michigan Heart Association).

Maternal and Fetal Platelet Responses and Adrenoceptor Binding Characteristics

1985 ◽  
Vol 53 (01) ◽  
pp. 095-098 ◽  
Author(s):  
C R Jones ◽  
R McCabe ◽  
C A Hamilton ◽  
J L Reid
Keyword(s):  
Adenylate Cyclase ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Binding Characteristics ◽  
Receptor Coupling ◽  
Threshold Response ◽  
Alpha Receptors ◽  
Maternal Responses ◽  
Epidural Anaesthetic

SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline.Alpha2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response- to increased circulating catecholamines during birth.

scholarly journals The (Patho)Biology of SRC Kinase in Platelets and Megakaryocytes

Medicina ◽  
2020 ◽  
Vol 56 (12) ◽  
pp. 633
Author(s):  
Lore De Kock ◽  
Kathleen Freson
Keyword(s):  
Platelet Activation ◽  
Knockout Mice ◽  
Missense Variant ◽  
Surface Receptors ◽  
Src Signaling ◽  
Normal Platelet ◽  
Fibrinogen Binding ◽  
Cellular Environment ◽  
Proplatelet Formation

Proto-oncogene tyrosine-protein kinase SRC (SRC), as other members of the SRC family kinases (SFK), plays an important role in regulating signal transduction by different cell surface receptors after changes in the cellular environment. Here, we reviewed the role of SRC in platelets and megakaryocytes (MK). In platelets, inactive closed SRC is coupled to the β subunit of integrin αIIbβ3 while upon fibrinogen binding during platelet activation, αIIbβ3-mediated outside-in signaling is initiated by activation of SRC. Active open SRC now further stimulates many downstream effectors via tyrosine phosphorylation of enzymes, adaptors, and especially cytoskeletal components. Functional platelet studies using SRC knockout mice or broad spectrum SFK inhibitors pointed out that SRC mediates their spreading on fibrinogen. On the other hand, an activating pathological SRC missense variant E527K in humans that causes bleeding inhibits collagen-induced platelet activation while stimulating platelet spreading. The role of SRC in megakaryopoiesis is much less studied. SRC knockout mice have a normal platelet count though studies with SFK inhibitors point out that SRC could interfere with MK polyploidization and proplatelet formation but these inhibitors are not specific. Patients with the SRC E527K variant have thrombocytopenia due to hyperactive SRC that inhibits proplatelet formation after increased spreading of MK on fibrinogen and enhanced formation of podosomes. Studies in humans have contributed significantly to our understanding of SRC signaling in platelets and MK.

Platelet-Activating Factor (PAF) in Internal Jugular Venous Blood of Migraine without aura Patients Assessed during Migraine Attacks

Cephalalgia ◽  
2004 ◽  
Vol 24 (8) ◽  
pp. 623-630 ◽  
Author(s):  
P Sarchielli ◽  
A Alberti ◽  
F Coppola ◽  
A Baldi ◽  
B Gallai ◽  
...  
Keyword(s):  
Platelet Activation ◽  
High Performance ◽  
Neurogenic Inflammation ◽  
Venous Blood ◽  
Platelet Activating Factor ◽  
Catheter Insertion ◽  
Reverse Phase Hplc ◽  
Opposite Trend ◽  
Serial Samples ◽  
Radioimmunoassay Method

The aim of the study was to verify the production of PAF and the activity of PAF acetyl-hydrolase (PAF-AH), the enzyme involved in the catabolism of this phospholipid mediator, in migraine attacks. Their levels were determined during migraine crises in serial samples of internal jugular venous blood taken from five migraine patients without aura, who were admitted to the hospital during the crises. Internal jugular venous blood samples were taken immediately after catheter insertion at 1, 2, and 4 h after attack onset, and within 2 h from its cessation. PAF was purified by high-performance liquid chromatography (HPLC) and determined by radioimmunoassay method. The enzymatic activity of PAF-AH was measured by reverse-phase HPLC, based on the derivatization with 7-diethylaminocoumarin-3-carbonylazide. In the internal jugular venous blood of migraine patients without aura (MO), an increase was observed in PAF levels, which was already evident at the time of catheter insertion (885.6 ± 82.8) and at the first hour (868.4 ± 65.24) (ANOVA: P < 0.0001). PAF levels remained elevated through the second (746.8 ± 82.95), fourth (700.6 ± 34.93) and sixth hours (644.4 ± 42.85), and then decreased at the end of the attack, reaching levels significantly lower than those measured at the time of catheter insertion (565.5 ± 38.34). The activity of PAF-AH showed an opposite trend with higher values at the first hour and significantly lower values at the second and fourth hours from the beginning of the migraine attack (ANOVA: P < 0.02). The increased production of PAF may account for persistent platelet activation during migraine crises, even in the presence of an increased production of nitric oxide (NO) end-products which, on the other hand, should instead intervene in counteracting and limiting platelet activation. Potential sources of PAF production are the endothelial cells from cerebral vessels, stimulated by trigeminal neuropeptides, platelets themselves, and mast cells, as suggested by the neurogenic inflammation model.

scholarly journals XVII. On the atomic weight of glucinum (Beryllium)

1883 ◽  
Vol 174 ◽  
pp. 601-613
Keyword(s):  
Specific Heat ◽  
Volatile Compound ◽  
Atomic Weight ◽  
Normal Number ◽  
Vapour Density ◽  
Atomic Heat ◽  
Lothar Meyer ◽  
Free Metal

I. Introductory. Ever since the discovery of glucinum by Vauquelin, in 1798, its atomic weight has been a disputed matter amongst chemists. Its discoverer considered that its oxide was a monoide, an opinion which was however strongly opposed by Berzelius, who wrote the oxide Gl 2 O 3 and the atomic weight 13⋅7 (O=16). The researches of Awdejew and Debrayt again turned the scale in favour of the earlier view, and as an atomic weight of 9⋅2 suited the properties of the metal in the tables of periodicy constructed by MM. Mendeleef and Lothar Meyer, this atomic weight has, up to quite recently, been generally accepted by chemists. As a welcome confirmation to this came a determination of the specific heat of the metal by Professor E. Reynolds, J who found that for its atomic heat to be near the normal number 6⋅0, its atomic weight must be 9⋅2 and not 13⋅8. Almost immediately afterwards a second determination of the specific heat was made by MM. Nilson and Petterson, who, however, obtained a result agreeing not with the lower atomic weight hut with the higher. The reasons for these conflicting opinions are to be found—first, in the anomalous position of glucinum among the elements; secondly, in the difficulties which surround the preparation of even small quantities of the free metal in a tolerably pure condition; and thirdly, in the fact that no volatile compound of glucinum is known of which the vapour density might be easily determined.

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