Optimization of therapy in patients with renal hypertension by stabilizing hemovascular hemostasis

Objective. To study the aggregation activity of platelets in patients with renal hypertension. Materials and methods. The research work was carried out on the basis of the nephrological department of the State Institution NMC RT “Shifobakhsh”. The study included 46 patients aged 25 to 60 years with chronic pyelo- and glomerulonephritis. The patients were divided into two equal groups: first, the control group received standard therapy in accordance with the clinical protocol of the Tajik Association of Nephrologists; second, the main group, along with complex pathogenetic therapy in order to stabilize the hemostasis system and improve endothelial dysfunction, used the drugs Tivortin (intravenously drip and then long-term per os Tivortin aspartate) and Rheosorbilact intravenously drip. In addition to the generally accepted studies of patients with kidney pathology, emphasis was placed on the criteria for platelet quality (number, mean platelet volume, platelet distribution index, thrombocyte and large erythrocyte ratio) and studies of the hemostasis system (fibrinogen, prothrombin time, activated partial thromboplastin time, prothrombin relation). Results. There were found the hemostasis in microvessels, increases of the blood viscosity, the activation of systemic thrombus formation, and the progression of endothelial dysfunction in patients with renal hypertension. The results of observation of the dynamics of platelet aggregation activity under the influence of the combination of the studied drugs in this category of patients prove an effective decrease in its level. It is also necessary to emphasize the antiplatelet effect of this combination in relation to the prevention of microthrombosis and the pronounced endothelioprotective effect in patients with renal pathology. Conclusions. The complex therapy of patients with renal hypertension with Tivortin and Rheosorbilact is an effective way to stabilize hemovascular hemostasis. The effects of this therapy contributed to the improvement of the clinical condition of the patients, and during repeated examinations, there was a stable preservation of the decrease in the level of platelet aggregation activity.

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Therapy with acetylsalicylic acid does not interfere with oral surgery

Open Medicine ◽

10.2478/s11536-013-0176-3 ◽

2013 ◽

Vol 8 (4) ◽

pp. 392-397 ◽

Cited By ~ 1

Author(s):

Damian Dudek ◽

Krzysztof Helewski ◽

Grzegorz Wyrobiec ◽

Marzena Harabin-Słowińska ◽

Grażyna Kowalczyk-Ziomek ◽

...

Keyword(s):

Heart Disease ◽

Platelet Aggregation ◽

Acetylsalicylic Acid ◽

Oral Surgery ◽

Thrombus Formation ◽

Heart Diseases ◽

Blood Platelets ◽

Control Group ◽

Drug Discontinuation ◽

Significant Group

AbstractThe acetylsalicylic acid (ASA) treatment is widespread therapeutic strategy in cardiology clinics. On the other hand, patients with heart diseases represent a significant group of cases in dental clinics. Accordingly, we studied the local hemostatic thrombus formation after dental tooth extractions (n=47) and other oral surgery treatment (n=13) in 60 patients with heart disease being on ASA therapy without drug discontinuation. In the control group free of ASA therapy it was: (n=24) and (n=6), respectively. In all studied patients, the aggregative activity of blood platelets by PFA-100 analyzer was assessed. It was found that 61.7% patients treated with ASA presented inhibition of platelets aggregation. Unexpectedly, in 35% of such patients, platelet aggregation function remained unchanged. In the control group, normal platelet aggregation was found in all subjects. It has been shown that ASA therapy has neutral effects on both thrombus formation and pain complications in patients with heart disease underwent tooth extraction and other oral surgery. Thus discontinuation of ASA therapy before surgery seems to be weakly validated.

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Endothelial dysfunction and platelet function disorder in hemostasis in development of hepatic fibrosis in children with autoimmune hepatitis

I P Pavlov Russian Medical Biological Herald ◽

10.23888/pavlovj2018264500-510 ◽

2018 ◽

Vol 26 (4) ◽

pp. 500-510

Author(s):

Ekaterina Yu. Konovalova ◽

Alla E. Lavrova ◽

Marina V. Presnyakova

Keyword(s):

Platelet Count ◽

Platelet Aggregation ◽

Endothelial Dysfunction ◽

Autoimmune Hepatitis ◽

Hepatic Fibrosis ◽

Von Willebrand Factor ◽

Metavir Score ◽

Aggregation Activity ◽

Von Willebrand ◽

Willebrand Factor

The purpose is: To assess the clinical relevance of the endothelial condition and platelet aggregation in the development of hepatic fibrosis in children with autoimmune hepatitis. Materials and Methods. 35 patients aged from 3 to 17 years old were studied, including 19 girls - (54%) and 16 boys - (46%). The 1st group consisted of 17 children with the degree of fibrosis F 0-2 acc. to the METAVIR score; the 2nd group consisted of 18 patients with the degree of fibrosis F 3-4 (METAVIR) acc. to the METAVIR score based on the indirect elastometry data in children of the 2nd group hepatic cirrhosis was diagnosed; the control group consisted of 15 children with health group I or II. The endothelium state and the platelet aggregation activity were assessed in all the patients. To test statistical hypotheses, the Mann-Whitney U test, the Spearman correlation coefficient and the Fisher criterion were used. The critical value of the significance level is assumed to be 0.05. Quantitative data are presented as: median and the first; third quartile of Me (Q1; Q3). Results. In children with autoimmune hepatitis some signs of the various-degree fibrosis formation were revealed in the ¾ of the examined. Patients of the 2nd group have a more aggressive course as compared to the 1st group: in the disease debut there were mainly expressed asthenoneurotic complaints (p = 0.021), manifestations of the jaundice syndrome (p = 0.014), more frequently hepatic-cell insufficiency (p = 0.045) is diagnosed and followed by complications of the disease (hypersplenism (p = 0.014), varicose veins of the esophagus (p = 0.003)). All children with autoimmune hepatitis have the endothelial dysfunction, the enhancing platelet aggregation activity. The degree of fibrosis correlates with the concentration of endothelin-1 (r = 0.4, p = 0.004), the von Willebrand factor (vWF) activity (r = 0.5, p <0.001), the platelet count (r = -0.5, p = 0.003). The determination of the endothelin-1 concentration, the von Willebrand factor activity and the platelet count may be used to assess the hepatopathy severity in children with autoimmune hepatitis. Conclusion. In children with autoimmune hepatitis the endothelial dysfunction and platelet disorders are revealed in the hemostasis system correlating with the severity of the pathological process.

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Inhaled Nitric Oxide Inhibits Platelet Aggregation after Pulmonary Embolism in Pigs

Anesthesiology ◽

10.1097/00000542-199702000-00013 ◽

1997 ◽

Vol 86 (2) ◽

pp. 387-393 ◽

Cited By ~ 37

Author(s):

Andre Gries ◽

Bernd W. Bottiger ◽

Joachim Dorsam ◽

Harry Bauer ◽

Jorg Weimann ◽

...

Keyword(s):

Nitric Oxide ◽

Pulmonary Embolism ◽

Platelet Aggregation ◽

Thrombus Formation ◽

Carbon Dioxide Concentration ◽

Right Ventricular Dysfunction ◽

Inhaled Nitric Oxide ◽

Control Group ◽

Maximum Decrease ◽

Inhaled No

Background Inhaled nitric oxide (NO) is reported to prolong bleeding time in animals and humans and to inhibit platelet aggregation in persons with acute respiratory distress syndrome. In pulmonary embolism (PE), inhibition of platelet aggregation appears useful because further thrombus formation may lead to right ventricular dysfunction that results in circulatory failure. In the present study, the effect of inhaled NO on platelet aggregation after acute massive PE was investigated. Methods After acute massive PE was induced in 25 anesthetized pigs by injecting microspheres, 5, 20, 40, and 80 parts per million inhaled NO were administered stepwise for 10 min each in 11 animals (NO group). In the control group (n = 14). NO was not administered. Adenosine diphosphate-induced initial and maximal platelet aggregation were measured before PE (10), immediately after induction of PE (PE), at the end of each 10-min NO inhalation interval (t10-t40), and 15 min after cessation of NO inhalation (t55) in the NO group, and at corresponding times in the control group, respectively. Results Two animals in the control group and one in the NO group died within 10 min after PE induction and were excluded from analysis. Peaking at t40 and t55, respectively, initial (-13 +/- 6%; P < 0.05) and maximal (+44 +/- 17%; P < 0.05) platelet aggregation increased significantly after PE in the control group. In contrast, NO administration after PE led to a significant decrease in initial (maximum decrease, -9 +/- 3% at t40; P < 0.05) and maximal (maximum decrease, -15 +/- 7% at t30; P < 0.05) platelet aggregation. In the NO group, platelet aggregation had returned to baseline levels again at t55. In addition, NO administration significantly decreased mean pulmonary artery pressure and significantly increased end-tidal carbon dioxide concentration and mean systemic blood pressure. Conclusions Inhaled NO has a systemic and rapidly reversible inhibitory effect on platelet aggregation after acute massive PE in pigs. This may be beneficial in treating acute massive PE.

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Comparative analysis of hemostasis system state indicators in severe COVID-19

Regional blood circulation and microcirculation ◽

10.24884/1682-6655-2021-20-4-87-94 ◽

2022 ◽

Vol 20 (4) ◽

pp. 87-94

Author(s):

I. A. Tikhomirova ◽

M. M. Ryabov

Keyword(s):

Platelet Aggregation ◽

Whole Blood ◽

Fibrinolytic Activity ◽

Blood Clotting ◽

Platelet Reactivity ◽

Thrombus Formation ◽

Venous Blood ◽

Clot Lysis ◽

Hemostasis System ◽

D Dimer

Introduction. Clinical experience in managing patients with a new coronavirus infection caused by the SARS-CoV-2 allowed to identify specific hemostasis disorders, and enables to introduce the concept of COVID-associated coagulopathy. The aim of the study was to assess the direction of coagulogram parameter changes, whole blood clotting parameters and characteristics of platelet and plasma hemostasis in patients with severe COVID-19. Materials and methods. The parameters of the hemostasis system were assessed using venous blood of 12 patients with severe COVID-19 and 16 healthy volunteers. The whole blood clotting process was investigated by low-frequency piezothromboelastography. The platelet count and indicators of spontaneous and ADP-induced platelet aggregation were estimated with the help of a laser platelet aggregation analyzer. Fibrinolytic activity of plasma, plasminogen activity, content of fibrinogen, D-dimer, PTT, APTT, PTI and INR were assessed. Results. An increased level of fibrinogen, a 6-fold increased D-dimer level, and increased PTT were found in patients with severe COVID-19. The patient platelets count was reduced by 51 % (p <0.05), spontaneous platelet aggregation remained at nearly normal level. Almost complete inhibition of ADP-induced platelet reactivity and inhibition of XIIa-dependent fibrinolysis was revealed, despite an increased by 19.3 % (p <0.05) plasminogen activity. Parameters of the whole blood coagulation process pointed a pronounced activation of platelet hemostasis, a significant intensification of the polymerization stage of clot formation and an increased intensity of clot lysis and retraction. Conclusion. The significant increase of D-dimer level and paradoxical inhibition of plasma fibrinolytic activity revealed by test of XIIa-dependent fibrinolysis (in contrast to the increased intensity of clot lysis when assessing the coagulation of whole blood) indicate the complex pathogenic mechanisms of coagulopathy caused by SARS-CoV-2 infection, and the involvement of blood cells and the vascular wall in the process of pathological thrombus formation.

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Experimental Study of the Effect of Photobiomodulation Therapy on the Regulation of the Healing Process of Chronic Wounds

International Journal of Photoenergy ◽

10.1155/2021/3947895 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Sergey B. Pavlov ◽

Nataliia M. Babenko ◽

Marina V. Kumetchko ◽

Olga B. Litvinova ◽

Rostyslav N. Mikhaylusov

Keyword(s):

Wound Healing ◽

Growth Factors ◽

Platelet Aggregation ◽

Chronic Wounds ◽

Healing Process ◽

Interleukin 10 ◽

Photobiomodulation Therapy ◽

Control Group ◽

Necrosis Factor Alpha ◽

Aggregation Activity

Currently, wound treatment is an urgent task of medicine around the world. In the process of wound healing, various types of cells are involved under the control and regulation of cytokines and growth factors. Disruption of the synchronization process between the various types of cells and intercellular mediators involved in the restoration of tissue damage can lead to impaired healing and the development of chronic wounds. Photobiomodulation (PBM) therapy promotes platelet activation and aggregation, reduces inflammation and oxidative stress, and accelerates cell migration and proliferation. PBM also induces the production of the extracellular matrix and the release of key growth factors, thereby improving tissue regeneration and accelerating wound healing. The aim of our work was to study the effect of photobiomodulation therapy on the regulation of reparative processes in chronic wounds monitored by biomarkers and platelet aggregation activity. 54 Wistar rats were divided into three groups. Intact animals were not manipulated. In animals of the control and experimental groups, a chronic wound was simulated by reproducing the conditions of local hypoxia and microcirculation disorders. The wounds of the experimental group received PBM therapy. The device Lika-therapist M (Ukraine) was used in a continuous mode at a wavelength of 660 nm, an output power of 10 mW, and an energy density of 1 J/cm2. The wounds of the animals in the control group were treated with sham. The animals were euthanized on days 3, 7, 14, and 28 after the surgery (6 animals, each from the control and experimental groups). Measurements of the levels of interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), the basic fibroblast growth factor (bFGF), and reactive oxygen species (ROS) were carried out by ELISA. Results revealed the multidirectional effect of PBM therapy on the expression of the studied biomarkers. The results of the histological examination indicated a positive effect of PBM therapy with the applied parameters on the repair processes of chronic wounds. We concluded that the use of PBM therapy made it possible to regulate disturbances in reparative processes by modulating ROS, cytokines, and platelet aggregation activity.

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Comparative characteristics of the hemostasis system state during hypothermic and early reactive periods of general freeze injury in rats

Kazan medical journal ◽

10.17750/kmj2017-989 ◽

2017 ◽

Vol 98 (6) ◽

pp. 989-993

Author(s):

N A Lycheva ◽

I I Shakhmatov ◽

S V Moskalenko

Keyword(s):

Cold Exposure ◽

Control Group ◽

System State ◽

Delayed Effect ◽

Profound Hypothermia ◽

Hemostasis System ◽

Hemostatic System ◽

Male Wistar Rats ◽

Aggregation Activity ◽

Experimental Group

Aim. To study the hemostasis system state in rats during hypothermic and post-hypothermic periods. Methods. Male Wistar rats (53 individuals) were used in the study. The animals from the experimental group underwent single immersion cooling in water at a temperature of 5 °C until profound hypothermia was reached, the control group of the animals was placed in water at a temperature of 30 °C. From the animals of the first group, blood was taken immediately after reaching profound hypothermia and from the second group - 24 hours after cooling was stopped. Results. Comparative analysis of the results showed that immediately after the end of a single cold exposure, significant increase in platelet aggregation activity occured, as well as appearance of thrombinemia markers in the bloodstream and inhibition of fibrinolytic system activity. 24 hours after the experimental exposure, these parameters returned to the initial values. When assessing the activity of external and internal ways of coagulation immediately after the termination of cooling, development of hypocoagulation was established, both with routine tests and from thromboelastography. After 24-hour period, hypocoagulation, recorded immediately after reaching the sought rectal temperature, persisted. Thus, after the end of a 24-hour period after cold exposure termination, most of the parameters of hemostatic system that had deviated immediately after the end of the experiment, returned to the normal level. The delayed effect of hypothermia in such cold exposure regimen manifested only by hypocoagulative shift at the initial stages of coagulation. Conclusion. Signs of abnormal hemostasiological blood properties, recorded immediately after the cooling termination, disappear within 24 hours, and only hypocoagulation persists in the blood.

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The role of disorders in the functional activity of platelets in the pathogenesis of microcirculatory disorders in patients with catarrhal gingivitis

10.34014/mpphe.2021-111-113 ◽

2021 ◽

Author(s):

V.N. Kitaeva ◽

A.V. Smolkina

Keyword(s):

Platelet Aggregation ◽

Key Words ◽

Functional Activity ◽

Maximum Degree ◽

Healthy Individuals ◽

Hemostasis System ◽

Comprehensive Examination ◽

Microcirculatory Disorders ◽

Aggregation Activity

A comprehensive examination of patients with chronic catarrhal gingivitis and with exacerbation of chronic catarrhal gingivitis with the inclusion of indicators of the microcirculatory link of the hemostasis system was carried out. In patients with exacerbation of chronic catarrhal gingivitis, platelet aggregation activity is increased compared to that in healthy individuals. This is accompanied by a statistically significant increase in the maximum degree of aggregation, a change in the time to reach the maximum degree of platelet aggregation Key words: platelet aggregation, catarrhal gingivitis, exacerbation of chronic catarrhal gingivitis.

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ADP Plays a Key Role in Thrombogenesis in Rats

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642759 ◽

1988 ◽

Vol 59 (02) ◽

pp. 225-230 ◽

Cited By ~ 63

Author(s):

J P Maffrand ◽

A Bernat ◽

D Delebassée ◽

G Defreyn ◽

J P Cazenave ◽

...

Keyword(s):

Platelet Aggregation ◽

Bleeding Time ◽

Thrombus Formation ◽

Vascular Wall ◽

Cyclooxygenase Inhibitors ◽

High Dose ◽

Silk Thread ◽

Dense Granules ◽

Prolonged Bleeding Time ◽

Venous Shunt

SummaryThe relative importance of ADP, arachidonic acid metabolites and serotonin as thrombogenic factors was evaluated in rats by comparing, after oral administration, the effects of two inhibitors of ADP-induced platelet aggregation (ticlopidine and PCR 4099), three cyclo-oxygenase inhibitors (aspirin, triflusal and indobufen) and a selective serotonin 5HT2 receptor antagonist (ketanserin) on platelet aggregation, in four platelet-dependent thrombosis models and on bleeding time. Platelet aggregation induced by ADP and collagen was completely inhibited by ticlopidine and PCR 4099 whereas only the collagen aggregation was reduced by the cyclo-oxygenase inhibitors. Ketanserin or a depletion of platelet serotonin by reserpine did not affect platelet aggregation. Ticlopidine and PCR 4099 greatly prolonged rat tail transection bleeding time. This is probably related to their known ability to inhibit ADP-mediated platelet aggregation. In contrast, the cyclooxygenase inhibitors did not affect bleeding time at all. Reserpine and ketanserin prolonged bleeding time by interfering with the action of serotonin on the vascular wall. Ticlopidine and PCR4099 were very potent antithrombotics in all the models. Aspirin, only at a high dose, inhibited poorly thrombus formation on a silk thread in an arterio-venous shunt, suggesting that the inhibition of cyclo-oxygenase was not responsible. Triflusal was inactive in all models while indobufen slightly reduced thrombus formation in the silk thread and metallic coil models. Ketanserin and reserpine reduced thrombus only in the metallic coil model. Thrombus formation was greatly reduced in fawn-hooded rats, which lack ADP in their platelet dense granules because of a genetic storage pool deficiency. Taken together, the results obtained with the drugs and with the fawn-hooded rats support the concept that ADP plays a key role in thrombogenesis in rats.

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Antithrombotic Effects and Bleeding Time Prolongation with Synthetic Platelet GPIIb/llla Inhibitors in Animal Models of Platelet-Mediated Thrombosis

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642390 ◽

1994 ◽

Vol 71 (01) ◽

pp. 095-102 ◽

Cited By ~ 43

Author(s):

Désiré Collen ◽

Hua Rong Lu ◽

Jean-Marie Stassen ◽

Ingrid Vreys ◽

Tsunehiro Yasuda ◽

...

Keyword(s):

Platelet Aggregation ◽

Bleeding Time ◽

Bolus Injection ◽

Cell Injury ◽

Ex Vivo ◽

Thrombus Formation ◽

Femoral Vein ◽

Thrombotic Occlusion ◽

Antithrombotic Effects

SummaryCyclic Arg-Gly-Asp (RGD) containing synthetic peptides such as L-cysteine, N-(mercaptoacetyl)-D-tyrosyl-L-arginylglycyl-L-a-aspartyl-cyclic (1→5)-sulfide, 5-oxide (G4120) and acetyl-L-cysteinyl-L-asparaginyl-L-prolyl-L-arginyl-glycyl-L-α-aspartyl-[0-methyltyrosyl]-L-arginyl-L-cysteinamide, cyclic 1→9-sulfide (TP9201) bind with high affinity to the platelet GPIIb/IIIa receptor.The relationship between antithrombotic effect, ex vivo platelet aggregation and bleeding time prolongation with both agents was studied in hamsters with a standardized femoral vein endothelial cell injury predisposing to platelet-rich mural thrombosis, and in dogs with a carotid arterial eversion graft inserted in the femoral artery. Intravenous administration of G4120 in hamsters inhibited in vivo thrombus formation with a 50% inhibitory bolus dose (ID50) of approximately 20 μg/kg, ex vivo ADP-induccd platelet aggregation with ID50 of 10 μg/kg, and bolus injection of 1 mg/kg prolonged the bleeding time from 38 ± 9 to 1,100 ± 330 s. Administration of TP9201 in hamsters inhibited in vivo thrombus formation with ID50 of 30 μg/kg, ex vivo platelet aggregation with an ID50 of 50 μg/kg and bolus injection of 1 mg/kg did not prolong the template bleeding time. In the dog eversion graft model, infusion of 100 μg/kg of G4120 over 60 min did not fully inhibit platelet-mediated thrombotic occlusion but was associated with inhibition of ADP-induccd ex vivo platelet aggregation and with prolongation of the template bleeding time from 1.3 ± 0.4 to 12 ± 2 min. Infusion of 300 μg/kg of TP9201 over 60 min completely prevented thrombotic occlusion, inhibited ex vivo platelet aggregation, but was not associated with prolongation of the template bleeding time.TP9201, unlike G4120, inhibits in vivo platelet-mediated thrombus formation without associated prolongation of the template bleeding time.

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The Inhibition of Platelet Aggregation by an Aorta Intima Extract

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647710 ◽

1974 ◽

Vol 32 (02/03) ◽

pp. 417-431 ◽

Cited By ~ 14

Author(s):

A. du P Heyns ◽

D. J van den Berg ◽

G. M Potgieter ◽

F. P Retief

Keyword(s):

Platelet Aggregation ◽

Degradation Products ◽

Adenosine Diphosphate ◽

Inhibitory Effect ◽

Protective Role ◽

Vascular Trauma ◽

Wear And Tear ◽

Sequential Addition ◽

Aggregation Activity

SummaryThe platelet aggregating activity of extracts of different layers of the arterial wall was compared to that of Achilles tendon. Arterial media and tendon extracts, adjusted to equivalent protein content as an index of concentration, aggregated platelets to the same extent but an arterial intima extract did not aggregate platelets. Platelet aggregation induced by collagen could be inhibited by mixing with intima extract, but only to a maximum of about 80%. Pre-mixing adenosine diphosphate (ADP) with intima extracts diminished the platelet aggregation activity of the ADP. Depending on the relationship between ADP and intima extract concentrations aggregating activity could either be completely inhibited or inhibition abolished. Incubation of ADP with intima extract and subsequent separation of degradation products by paper chromatography, demonstrated a time-dependent breakdown of ADP with AMP, adenosine, inosine and hypoxanthine as metabolic products; ADP removal was complete. Collagen, thrombin and adrenaline aggregate platelets mainly by endogenous ADP of the release reaction. Results of experiments comparing inhibition of aggregation caused by premixing aggregating agent with intima extract, before exposure to platelets, and the sequential addition of first the intima extract and then aggregating agent to platelets, suggest that the inhibitory effect of intima extract results from ADP breakdown. It is suggested that this ADP degradation by intima extract may play a protective role in vivo by limiting the size of platelet aggregates forming at the site of minimal “wear and tear” vascular trauma.

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