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

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.

Prevalence of allelic and genotypic variants of the rs1143627 polymorphism in the IL1β gene among patients with typhoid

2020 ◽  
Vol 18 (3) ◽  
pp. 126-130
Author(s):  
D.B. Mirzajonova ◽  
◽  
H.Ya. Karimov ◽  
G.K. Abdukhalilova ◽  
K.T. Boboev ◽  
...  
Keyword(s):  
Typhoid Fever ◽  
Key Words ◽  
Main Group ◽  
Minor Allele ◽  
Control Group ◽  
Healthy Individuals ◽  
Allele Detection ◽  
Generic Structure

Objective. To evaluatethe role of allelic and genotypic variants of gene IL1β polymorphism rs1143627 in susceptibility to typhoid fever (TF). Materials and methods. 41 patients with TF and 84 chronic carriers of S. typhi were endrolled in the study. Control group included 91 healthy individuals, All of the individuals under study were Uzbeks. DNA samples were isolated from peripheric blood with the kit Ribo-sorb (AmpliSens®, Russia). Genotyping of polymorphism rs1143627 of gene IL1β was carried out by the standard PCR using kits “SNP-Express” (LLC NPF “LITECH”, Russia) according to the instruction of manufacturer. Results. The domination of allele 31T was found in the main group (patients and carriers). Its frequency was significantly lower in comparison with the control group (51.2% and 67.0%, respectively; χ2 = 10.8; p = 0.001). Minor allele -31С cytokine IL1β, on the contrary was detected more frequently in patients with TF (48.8%), than in the control group (33.0%) in χ2 = 10.8 and p = 0.001. Calculated relative chance of this allele detection in the main group in comparison with control group was OR = 1.9 in 95% CI 1.304-2.88. Conclusion. Genotypic variant C/C of polymorphism rs1143627 of the gene IL1β made a certain contribution into forming of generic structure of susceptibility to S. typhi. Risk of susceptibility of macro organism to pathogen in the presence of this genotype is higher more than 2.5 times (χ2 = 4.3; p = 0.04; CI 95% 1.037–7.359). Key words: Typhoid fever, bacteria carrier, bacteria S. typhi, polymorphism rs1143627 of the gene IL1β

Normalization of microbiota in gynecological practice. Criteria for selection of probiotic

2017 ◽  
pp. 21-26
Author(s):  
N.A. Tsubanova ◽  
◽  
T.V. Sevastyanova ◽  
E.S. Tsubanova ◽  
◽  
...  
Keyword(s):  
Key Words ◽  
Human Health ◽  
Functional Activity ◽  
Evidence Base ◽  
The State ◽  
Sufficient Evidence ◽  
Detailed Consideration ◽  
Criteria For Selection ◽  
Selection Of

The article analyzes modern research on the functional activity of microbiota and its relationship to the state of human health. A detailed consideration of the role of dysbiosis in gynecological practice. Requirements for modern probiotic drugs are given. It is established that one of the drugs that meet modern criteria is the multi-probiotic probiotic Probiz Femina (Organosyn), for which a sufficient evidence base has been accumulated, which makes it an effective and safe probiotic for many cohorts of patients. Key words: microbiota, dysbiosis, multi-probiotic probiotic Probiz Femina.

Research of spontaneous and stimulated functional activity of platelets in patients with different types of atrial fibrillation

2021 ◽  
Vol 66 (1) ◽  
pp. 35-41
Author(s):  
O. N. Ogurkova ◽  
T. E. Suslova ◽  
R. E. Batalov
Keyword(s):  
Atrial Fibrillation ◽  
Comparative Analysis ◽  
Platelet Aggregation ◽  
Functional Activity ◽  
Reaction Medium ◽  
Thromboembolic Complications ◽  
Different Types ◽  
Β Blockers ◽  
Aggregation Activity ◽  
Function Testing

Platelet function testing is widely used to diagnose disorders of the cellular link of hemostasis. The study of platelet aggregation activity is relevant for the prevention of thromboembolic complications in atrial fibrillation and monitoring the effectiveness and safety of therapy. In this study, a comparative analysis of spontaneous and stimulated platelet aggregation in groups of patients with two types of atrial fibrillation was performed - paroxysmal and persistent. The effect of β-adrenoblocker therapy on platelet aggregation activity in patients with atrial fibrillation was also studied. Platelet aggregation activity was studied using the method of G. Born in the modification of Z.A. Gabbasov on a two-channel laser analyzer “Biola”. Collagen at a concentration of 2 mg / ml and adrenaline in a concentration range of 2.5-10 μg / ml were used as aggregation-promoting agents. It has been established that spontaneous aggregation potential and collagen-induced platelet aggregation depend on the type of atrial fibrillation, as well as on the presence or absence of β-blockers in therapy. The response of platelets to stimulation with adrenaline depends, first of all, on the type of atrial fibrillation and the concentration of adrenaline in the reaction medium. The most significant changes were noted in the group of patients with a paroxysmal form atrial fibrillation, taking β-blockers in therapy.

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

2020 ◽  
pp. 90-90
Author(s):  
N.Kh. Bobieva ◽  
S.Kh. Gadoev ◽  
I.M. Rashidov
Keyword(s):  
Platelet Aggregation ◽  
Endothelial Dysfunction ◽  
Thrombus Formation ◽  
Renal Hypertension ◽  
Research Work ◽  
State Institution ◽  
Control Group ◽  
Hemostasis System ◽  
Pathogenetic Therapy ◽  
Aggregation Activity

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.

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

The Inhibition of Platelet Aggregation by an Aorta Intima Extract

1974 ◽  
Vol 32 (02/03) ◽  
pp. 417-431 ◽  
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.

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.

Testosterone Potentiation of Ionophore and ADP Induced Platelet Aggregation : Relationship to Arachidonic Acid Metabolism

1981 ◽  
Vol 46 (02) ◽  
pp. 538-542 ◽  
Author(s):  
R Pilo ◽  
D Aharony ◽  
A Raz
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Unsaturated Fatty Acids ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Arachidonic Acid Metabolism ◽  
Ionophore A23187 ◽  
Low Concentrations ◽  
Induced Aggregation

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.

Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate

1985 ◽  
Vol 54 (03) ◽  
pp. 612-616 ◽  
Author(s):  
A J Carter ◽  
S Heptinstall
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Thromboxane B2 ◽  
Lipoxygenase Inhibitor ◽  
Thromboxane Synthase Inhibitor ◽  
Synthase Inhibitor

SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature and concentration of the aggregating agent used. The various inhibitors of thromboxane synthesis - aspirin and flurbiprofen (cyclo-oxygenase inhibitors), BW755C (a cyclo-oxygenase and lipoxygenase inhibitor) and dazoxiben (a selective thromboxane synthase inhibitor) - did not markedly inhibit aggregation. Results obtained using apyrase showed that adenosine diphosphate contributed to the aggregation process, and that its role must be acknowledged when devising means of inhibiting platelet aggregation in vivo.

Collagen-Induced Platelet Aggregation: -Evidence Against the Essential Role of Platelet Adenosine Diphosphate

1979 ◽  
Vol 42 (04) ◽  
pp. 1193-1206 ◽  
Author(s):  
Barbara Nunn
Keyword(s):  
Platelet Aggregation ◽  
Time Course ◽  
Essential Role ◽  
Atp Release ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
High Doses ◽  
Induced Aggregation

SummaryThe hypothesis that platelet ADP is responsible for collagen-induced aggregation has been re-examined. It was found that the concentration of ADP obtaining in human PRP at the onset of aggregation was not sufficient to account for that aggregation. Furthermore, the time-course of collagen-induced release in human PRP was the same as that in sheep PRP where ADP does not cause release. These findings are not consistent with claims that ADP alone perpetuates a collagen-initiated release-aggregation-release sequence. The effects of high doses of collagen, which released 4-5 μM ADP, were not inhibited by 500 pM adenosine, a concentration that greatly reduced the effect of 300 μM ADP. Collagen caused aggregation in ADP-refractory PRP and in platelet suspensions unresponsive to 1 mM ADP. Thus human platelets can aggregate in response to collagen under circumstances in which they cannot respond to ADP. Apyrase inhibited aggregation and ATP release in platelet suspensions but not in human PRP. Evidence is presented that the means currently used to examine the role of ADP in aggregation require investigation.

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