Prostacyclin Prevents Endothelial & Platelet Damage During Haemodialysis

1981 ◽  
Author(s):  
J H Turney ◽  
N Dodd ◽  
M J Weston
Keyword(s):  
Cardiovascular Disease ◽  
Factor Viii ◽  
Antithrombin Iii ◽  
Endothelial Damage ◽  
Atherosclerotic Cardiovascular Disease ◽  
Vascular Endothelial ◽  
Blood Components ◽  
Prothrombotic State ◽  
At Iii ◽  
Extracorporeal Circuits

We have previously demonstrated that prostacyclin (PGI) enhances the biocompatibility of extracorporeal circuits. Dialysis with & without PGI were studied in 17 patients. We measured platelet count, (β-thromboglobulin, factor VIII related antigen, & Antithrombin III (Bick method). Results are presented as percentage change + SEM of initial values.The change in all values during dialysis with heparin alone was significant (p<0.005). Additional PGI prevented any change (p<0.0001 compared with heparin at 300 minutes). We conclude that platelet activation & consumption persists throughout dialysis with heparin alone. The rise in factor VIII-RA & AT III reflects vascular endothelial damage induced by the reinfusion of activated blood components. Thus PGI not only protects platelets but also prevents dialysis-induced vascular endothelial damage. Longterm use of PGI should tend to reverse the prothrombotic state in dialysed uraemic patients and may therefore reduce their risk of atherosclerotic cardiovascular disease.

Regular Haemodialysis Therapy (RDT) Induces A Prothrombotic State

1979 ◽  
Author(s):  
J. Turney ◽  
H.F. Woods ◽  
M.J. Weston
Keyword(s):  
Factor Viii ◽  
Antithrombin Iii ◽  
Coagulation Factors ◽  
Prothrombotic State ◽  
Factor Viii Related Antigen ◽  
Coagulant Activity ◽  
At Iii ◽  
Thrombin Activation ◽  
The Mean ◽  
Circulating Levels

To determine whether activation of coagulation factors and platelets, reported during haemodialysis results in a prothrombotic state we have studied indices of coagulability in 15 undialysed and 32 dialysed uraemic patients. Mean plasma fibrinogen (g/1) in uraemic patients (3.53) was significantly higher than in controls (2.45) and rose further in dialysed patients (3.81). Factor VIII coagulant activity (CA) was greater in dialysed (202 ± 15.9%) than in undialysed uraemic patients (184 ± 14.2%) both being significantly greater than control (84 ± 3.9). Similarly Factor VIII related antigen (RA) was higher in dialysed patients (216 ± 18.5%) than uraemics (156 ± 9.6%) (control = 94 ± 5.6%). The mean RA/CA ratio and the frequency of a high RA/CA ratio (< 1.5), an index of thrombin induced consumption of Factor VIII-CA and intravascular coagulation, were higher in dialysed than nondialysed patients.Despite the higher circulating levels of procoagulants and the evidence of thrombin activation the availability of heparin cofactor-antithrombin III (AT III) was lower in dialysed (154%) than in uraemic patients (159%) though in both groups AT III levels were higher than in controls (100%).These results indicate that RDT is associated with a prothrombotic state which is not completely compensated for by an increase in antithrombin III.

Personalized approach to procurement of hemocomponents taking into account hemostasis characteristics of donors

2018 ◽  
Author(s):  
А.Ф. Кубиддинов ◽  
Д.С. Саидов ◽  
М.З. Тагожонов ◽  
А.А. Одинаев ◽  
З.Ф. Тагожонов ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Blood Clotting ◽  
International Normalized Ratio ◽  
Blood Components ◽  
Transfusion Therapy ◽  
At Iii ◽  
Personalized Approach ◽  
Von Willebrand ◽  
Fibrinogen Content

Цель исследования: изучение параметров гемостаза у доноров для оптимизации использования компонентов крови у пациентов с нарушениями свертывания крови. Материалы и методы. Проанализированы результаты коагулологического исследования крови у 200 доноров. Контрольную группу составили 50 человек — здоровые люди (добровольцы), не доноры в возрасте от 20 до 60 лет. Измеряли: время свертывание крови по Ли-Уайту, активированное частичное тромбопластиновое время, международное нормализованное отношение, агрегацию тромбоцитов, антитромбин III (АТ-III), содержание фибриногена по Клаусу, фактор фон Виллебранда (ФВ), активность фактора VIII. Рассчитывали среднюю арифметическую и среднюю ошибку средней арифметической (М ± m), для оценки значимости различий средних величин использовали t-критерий Стьюдента, различия считали статистически значимыми при р < 0,05. Результаты. Оценка показателей гемостаза показала как развитие у доноров склонности к гиперкоагуляции, так и компенсаторную активацию антикоагулянтной системы. В зависимости от возраста и количества кровосдач агрегация тромбоцитов, АТ-III, содержание фибриногена, активность ФВ и фактора VIII в заготовленных компонентах крови получаются различными. Заключение. Трансфузионная терапия коагулопатий может быть оптимизирована за счет применения компонентов крови, целенаправленно заготовленных с учетом характера нарушений свертывания крови у реципиента. Aim: to optimize the usage of blood components in patients with coagulopathy we analyze some hemostasis parameters in donors. Materials and methods. In 200 donors and 50 healthy volunteers (aged from 20 to 60 years old) we analyzed hemostatic parameters: whole blood clotting time, activated partial thromboplastin time, international normalized ratio, platelet aggregation, antithrombin III (AT-III), Claus fibrinogen content, activity of von Willebrand factor (VWF) and factor VIII. The results obtained presented as M ± m. Statistical diff erences by Student test were considered as signifi cant for p < 0,05. Results. All donors had the tendency to hypercoagulation with compensatory activation of anticoagulant system. Depending on the age and number of blood donations, obtained blood components were diff erent in platelet aggregation, AT-III level, fibrinogen content, activity of VWF and factor VIII. Conclusion. Transfusion therapy of coagulopathies can be optimized through the use of blood components purposefully prepared taking into account the nature of blood clotting disorders in the recipient.

Development and characterization of an automated assay of effective heparin activity in plasma.

1987 ◽  
Vol 33 (9) ◽  
pp. 1630-1634 ◽  
Author(s):  
J F Pierson-Perry ◽  
D M Obzansky ◽  
J P Mizzer
Keyword(s):  
Antithrombin Iii ◽  
Factor Xa ◽  
Sole Source ◽  
Chromogenic Substrate ◽  
Blood Components ◽  
Automated Assay ◽  
At Iii ◽  
Assay Result ◽  
Heparin Activity

Abstract We describe a fully automated assay for determining effective heparin activity in plasma, based on heparin-catalyzed inhibition of Factor Xa (EC 3.4.21.6) by antithrombin III (AT III). Residual Factor Xa is determined kinetically by the Du Pont aca discrete clinical analyzer with a chromogenic substrate and is inversely related to heparin activity. Because the test plasma is the sole source of AT III, the assay result is dependent on AT III activity and reflects effective rather than total heparin activity. The assay range is 20-1200 USP units/L, and the assay shows equivalent sensitivity to standard and low-molecular-mass heparins. Within-run reproducibility (CV) is 1.6% at 390 units/L. There was no interference from common blood components or drugs. Results agreed well with those by the Coatest heparin kit (Kabi) adapted to the Cobas-Bio analyzer (r = 0.85, n = 122).

scholarly journals Antithrombin III and Hypercoagulability in Smokers

1977 ◽  
Author(s):  
R. Losito ◽  
D. Nathan ◽  
H. Gattiker ◽  
B. Longpré
Keyword(s):  
Factor Viii ◽  
Thrombin Generation ◽  
Antithrombin Iii ◽  
Intravascular Coagulation ◽  
Coagulation Tests ◽  
At Iii ◽  
History Of ◽  
Generation Test

It is known that various coagulation tests such as the thromboplastin generation test (TGT), thrombin generation (TG), levels of factor VIII or antithrombin III have been found to be abnormal in individuals with intravascular coagulation or having an increased tendancy to thrombosis. The aim of this study was to evaluate the role of the TGT, TG, factor VIII and antithrombin III assays in the diagnosis of possible mild intravascular coagulation in patients undergoing cardiac catheterization who had a history of smoking. In addition to these four tests, a routine coagulogram was performed for a total of 13 tests. It appeared that smokers had more abnormal tests (7.3/patient) than the controls (3.3/patient). The greatest association was between TGT and TG (29.6%) and TG and AT-III (25.9%). If by definition, hypercoagulability is present where 3 or more of these 4 mentioned tests were abnormal, then five patients were found to be in this category; all, except one, formed clots. In the patients (50) with a history of smoking, a third were found to have the TGT and the TG abnormal; however, the most striking observation in this group was in the antithrombin III where it was noted to be low in forty-five percent of the patients compared to the controls (patients having catheterization and were non-smokers) whose antithrombin III was found to be decreased in only five percent of the individuals. It is concluded that determination of antithrombin III may be of more importance in assisting the detection of hypercoagulability, especially in the smoking population, than the TGT, TG, or factor VIII.

Role of Microparticles in Cardiovascular Disease: Implications for Endothelial Dysfunction, Thrombosis, and Inflammation

Hypertension ◽  
2021 ◽  
Vol 77 (6) ◽  
pp. 1825-1844
Author(s):  
Leslie Marisol Lugo-Gavidia ◽  
Dylan Burger ◽  
Vance B. Matthews ◽  
Janis M. Nolde ◽  
Márcio Galindo Kiuchi ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Causal Link ◽  
Endothelial Damage ◽  
Special Focus ◽  
Vascular Health ◽  
Biological Processes ◽  
Prothrombotic State ◽  
Pathological Conditions ◽  
Relevant Role

Microparticles are small cell vesicles that are derived from the cell membrane in response to different biological processes. There is growing evidence supporting the association between microparticles and cardiovascular disease, as their pathophysiology commonly includes endothelial damage and chronic inflammation which also promote a prothrombotic state. The direct causal link between the release of the different subtypes of microparticles and their implications on physiological and pathological conditions is still not completely elucidated. However, evidence suggests microparticles released from platelets, leukocytes, and endothelium may help to evaluate vascular health as they have a relevant role in inflammation, endothelial function, and thrombosis. This review aims to provide a short overview of the biogenesis, characteristics, and detection methodology of microparticles with a special focus on their possible implication in cardiovascular settings.

The Role of Venom Haemorrhagin in Spontaneous Bleeding in Bothrops jararaca Envenoming

1992 ◽  
Vol 67 (04) ◽  
pp. 484-488 ◽  
Author(s):  
A S Kamiguti ◽  
F P Rugman ◽  
R D G Theakston ◽  
F O S Franca ◽  
H Ishii ◽  
...  
Keyword(s):  
Antithrombin Iii ◽  
Clinical Signs ◽  
Endothelial Damage ◽  
Vascular Endothelial ◽  
Spontaneous Bleeding ◽  
Bothrops Jararaca ◽  
Thrombin Antithrombin Iii Complex ◽  
Very High ◽  
D Dimer

SummaryThirty-eight patients bitten by Bothrops jararaca were investigated. Twenty-six had signs of local or systemic haemorrhage. Twenty-two of these had incoagulable blood, and these patients were found to have low fibrinogen levels (mean 0.17 ± 0.03 g/1), thrombocytopenia, very high thrombin-antithrombin III complex (850 ± 184 pg/1) and D-dimer (170 ± 44 μg/ml) antigen levels. Serum venom haemorrhagin levels were significantly higher in patients with clinical signs of haemorrhage (36.4 ± 6.4 ng/ml) than those without (11.7 ± 3.7 ng/ml; p <0.002). Twelve out of 13 patients with thrombocytopenia were bleeding. High levels of thrombomodulin (22.3 ± 1.5 ng/ml) and haemorrhagin (35.7 ± 7.7 ng/ml) were detected in these 12 patients, suggesting vascular endothelial damage. Haemorrhagin levels also correlated inversely with platelet count in these patients. It was concluded that thrombocytopenia is one of the main causes of bleeding inB. jararaca victims, possibly as a result of venom haemorrhagin activity.

scholarly journals MARKERS OF VASCULAR TONE AND INFLAMMATION IN PERSONS EXPOSED TO MERCURY

2019 ◽  
Vol 98 (10) ◽  
pp. 1079-1084 ◽  
Author(s):  
Olga V. Naumova ◽  
I. V. Kudaeva ◽  
L. B. Masnavieva ◽  
O. A. Dyakovich
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Vascular Tone ◽  
Endothelial Damage ◽  
Vascular Endothelial ◽  
Cross Sectional Survey ◽  
Cross Sectional ◽  
Mercury Intoxication ◽  
Chronic Mercury Intoxication ◽  
Regulation Of Vascular Tone

Introduction. Endothelial dysfunction (ED) is an important link in the development of cardiovascular disease. There is evidence that exposure to mercury and its compounds can be a risk factor for the development of ED. The aim - the study of endothelial dysfunction markers involved in the regulation of vascular tone, inflammation, and vascular endothelial damage in patients with cardiovascular disease, the exposed and unexposed mercury. Material and Methods. In persons exposed due to their occupational activities with metallic mercury, who had been working for over five years, people with newly diagnosed chronic mercury intoxication and patients with chronic mercury intoxication in the long post-exposure period, and the persons are not exposed mercury a cross-sectional survey was conducted using biochemical methods Results. In examinees there have been revealed changes in the content of biochemical indices of ED - reducing nitrogen oxide, an elevated level of endothelin-1, angiotensin II, histamine, hsCRP, homocysteine. There has been established a breach in the content of ED markers that are pathogenic factors in the development of ED and, as a consequence, the development of cardiovascular disease in chronic mercury exposure. Conclusion. In persons exposed to mercury there were the most pronounced changes in the regulation of vascular tone, which may be one of the factors in the development of vascular disease. At the same time the importance of inflammation indices and vascular endothelial damage plays a secondary role.

Molekularbiologische Grundlagen und Diagnostik der hereditären Defekte von Antithrombin III, Protein C und Protein S

2002 ◽  
Vol 22 (02) ◽  
pp. 57-66
Author(s):  
I. Witt
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
Klinische Relevanz ◽  
At Iii

ZusammenfassungDie enormen Fortschritte in der Molekularbiologie in den letzten Jahren ermöglichten sowohl die Aufklärung der Nukleotidsequenzen der Gene für Antithrombin III (AT III), Protein C (PROC) und Protein S (PROS) als auch die Identifizierung zahlreicher Mutationen bei hereditären Defekten dieser wichtigen Inhibitoren des plasmatischen Gerinnungssystems. Da die Gene für AT III (13,8 kb) und PROC (11,2 kb) nicht groß und relativ leicht zu analysieren sind, gibt es bereits umfangreiche »databases« der Mutationen (50, 73). Für AT III sind 79 und für PROC 160 unterschiedliche Mutationen beschrieben.Sowohl beim AT-III-Mangel als auch beim Protein-C-Mangel hat die Mutationsaufklärung neue Erkenntnisse über die Struktur-Funktions-Beziehung der Proteine gebracht. Beim Protein-C-Mangel steht die klinische Relevanz der DNA-Analyse im Vordergrund, da die Diagnostik des Protein-C-Mangels auf der Proteinebene nicht immer zuverlässig möglich ist.Das Protein-S-Gen ist für die Analytik schwer zugänglich, da es groß ist (80 kb) und außerdem ein Pseudogen existiert. Es sind schon zahlreiche Mutationen bei Patienten mit Protein-S-Mangel identifiziert worden. Eine Database ist bisher nicht publiziert. Die klinische Notwendigkeit zur Mutationsaufklärung besteht ebenso wie beim Protein-C-Mangel. Es ist zu erwarten, dass zukünftig die Identifizierung von Mutationen auch beim Protein-S-Mangel beschleunigt vorangeht.

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

Immunologic Studies of Antithrombin III Heparin Cofactor in the Newborn

1978 ◽  
Vol 39 (03) ◽  
pp. 624-630 ◽  
Author(s):  
W E Hathaway ◽  
L L Neumann ◽  
C A Borden ◽  
L J Jacobson
Keyword(s):  
Gestational Age ◽  
Antithrombin Iii ◽  
Newborn Infants ◽  
Term Infant ◽  
Sick Newborn ◽  
At Iii ◽  
Thrombotic Complications ◽  
Low Levels ◽  
Collection Methods ◽  
Made In

SummarySerial quantitative immunoelectrophoretic (IE) measurements of antithrombin III heparin cofactor (AT III) were made in groups of well and sick newborn infants classified by gestational age. Collection methods (venous vs. capillary) did not influence the results; serum IE measurements were comparable to AT III activity by a clotting method. AT III is gestational age-dependent, increasing from 28.7% of normal adult values at 28-32 weeks to 50.9% at 37-40 weeks, and shows a gradual increase to term infant levels (57.4%) by 3-4 weeks of age. Infants with the respiratory distress syndrome (RDS) show lower levels of AT III in the 33-36 week group, 22% vs. 44% and in the 37-40 week group, 33.6% vs. 50.9%, than prematures without RDS. Infants of 28-32 week gestational age had only slight differences, RDS = 24%, non-RDS = 28.7%. The lowest levels of AT III were seen in patients with RDS complicated by disseminated intravascular coagulation and those with necrotizing enterocolitis. Crossed IE on representative infants displayed a consistent pattern which was identical to adult controls except for appropriate decreases in the amplitude of the peaks. The thrombotic complications seen in the sick preterm infant may be related to the low levels of AT III.

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