scholarly journals Platelet aggregation in hypothyroidism and graves’ disease

2015 ◽  
Vol 96 (5) ◽  
pp. 742-744 ◽  
Author(s):  
M V Chepis ◽  
E S Ral’chenko ◽  
A A Klimenova ◽  
I V Ral’chenko
Keyword(s):  
Platelet Aggregation ◽  
Thyroid Dysfunction ◽  
Formation Rate ◽  
Maximum Size ◽  
Activated Partial Thromboplastin Time ◽  
Control Group ◽  
Graves Disease ◽  
Dynamic Measurements ◽  
Healthy Donors ◽  
Platelet Aggregates

Aim. To study platelet aggregation in subclinical and symptomatic hypothyroidism and Graves’ disease. Methods. The results of clinical and laboratory study of 50 patients with hypothyroidism and 20 patients with Graves’ disease are described. To access platelets aggregation function aggregatogramms were decoded by setting the maximum aggregation value; maximum aggregation rate and platelet aggregates maximum size were evaluated according to the results of the dynamic measurements on aggregometer. A control group consisted of 40 healthy donors. Results. Patients with subclinical and symptomatic hypothyroidism had prolonged activated partial thromboplastin time, reflecting the propensity for hypocoagulation, reduced total platelets number, spontaneous and ADP-induced platelet aggregation, aggregates formation rate and their maximum size. Changes were more pronounced in patients with Graves’ disease: weakening of platelet component of hemostasis, reduction of the platelets total number and the maximum size of platelet aggregates, significant reduction of the rate to reach the maximum size of platelet aggregates and platelet aggregation were observed. Conclusion. Thyroid dysfunction is accompanied by dysfunction of hemocoagulation processes, signs of chronic disseminated intravascular coagulation syndrome; these changes are clinically more severe in patients with Graves’ disease.

Arginine-containing peptides and their influenceon normal hemostatic parameters in rats

2019 ◽  
Author(s):  
Э.Я. Рогозинская ◽  
М.Е. Григорьева ◽  
Л.А. Ляпина
Keyword(s):  
Body Weight ◽  
Platelet Aggregation ◽  
Activated Partial Thromboplastin Time ◽  
Control Group ◽  
Antiplatelet Activity ◽  
Nacl Solution ◽  
White Rats ◽  
Anticoagulation System

Введение. В ранних исследованиях была выявлена способность аргининсодержащих пептидов глипролинового ряда в условиях in vitro оказывать антикоагулянтные и суммарные фибринолитические эффекты на плазму крови лабораторных крыс. Цель исследования: изучение действия аргининсодержащих глипролинов HisPheArgTrpProGlyPro (HFRWPGP), ThrLysProArgProGlyPro (TKPRPGP), ArgGluArgProGlyPro (RERPGP) на параметры системы гемостаза крыс в условиях in vivo в норме и сравнительный анализ эффектов исследуемых пептидов с глипролином (PGP). Материалы и методы. В работе использовали пептиды HFRWPGP (АКТГ(69)PGP), TKPRPGP (Селанк), RERPGP и PGP. В опытах 20 белым лабораторным крысам интраназально вводили по 0,02 мл раствора каждого из пептидов в дозе 1 мкг/кг массы тела (3 опытных группы) или 0,85 раствора NaCl (контрольная группа) через каждые 24 ч в течение 7 суток (168 ч). Влияние пептидов на параметры гемостаза исследовали тромбоэластографическим методом, в тестах активированного частичного тромбопластинового времени и агрегации тромбоцитов, а также определяли фибринолитическую активность крови на нестабилизированном фибрине. Результаты. Каждый из исследованных препаратов обнаруживал антикоагулянтную, фибринолитическую, антитромбоцитарную активности. Противосвертывающие эффекты проявлялись через 20 ч после последнего введения и сохранялись на протяжении 168 ч. Наибольшим эффектом обладали пептиды, в состав которых входил аргинин ArgGluArgProGlyPro и Селанк. Заключение. Аминокислота аргинин в составе олигопептидов глипролинового ряда способствует усилению активации противосвертывающей системы. Introduction. Early in vitro studies revealed anticoagulant and fibrinolytic effects of argininecontaining glyprolins on plasma in rats. Aim: to study the effects of argininecontaining glyprolines HisPheArgTrpProGlyPro (HFRWPGP), ThrLysProArgProGlyPro (TKPRPGP), ArgGluArgProGlyPro (RERPGP) on rats hemostasis in vivo in normal conditions and to compare the effects of test peptides with glyproline (PGP). Materials and methods. The following peptides were used: HFRWPGP (ACTH(69)PGP), TKPRPGP (Selank), RERPGP and PGP. In experiments 20 white rats were intranasally injected with 0.02 ml of each peptide solution in a dose of 1 g/kg body weight (3 experimental groups) or 0.85 NaCl solution (control group) every 24 hours for 7 days (168 hours). The effects of peptides on hemostatic parameters were investigated by thromboelastographic method, by activated partial thromboplastin time and platelet aggregation, also fibrinolytic blood activity on nonstabilized fibrin was determined. Results. All tested peptides showed anticoagulant, fibrinolytic, antiplatelet activity. Anticoagulant effects manifested 20 hours after the last injection and persisted for 168 hours. Argininecontaining ArgGluArgProGlyPro and Selank showed the greatest effect. Conclusion. Arginine as a part of argininecontaining glyprolines intensified the activation of anticoagulation system.

Dietary Calcium Supplementation Suppresses Bone Formation in Magnesium-Deficient Rats

2006 ◽  
Vol 76 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Matsuzaki ◽  
Misao Miwa
Keyword(s):  
Bone Formation ◽  
Calcium Supplementation ◽  
Control Diet ◽  
Formation Rate ◽  
Dietary Calcium ◽  
Mineral Apposition Rate ◽  
Control Group ◽  
Deficient Diet ◽  
Bone Formation Rate ◽  
Male Wistar Rats

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg - and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg - and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg - and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg - group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.

Ticlopidine Facilitates the Deaggregation of Human Platelets Aggregated by Thrombin

1994 ◽  
Vol 71 (01) ◽  
pp. 091-094 ◽  
Author(s):  
M Cattaneo ◽  
B Akkawat ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
C Cimminiello ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Human Platelet ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
Before And After ◽  
Normal Human ◽  
Platelet Aggregates ◽  
Induced Aggregation

SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d. Before and after ticlopidine, platelets stimulated with 1 U/ml thrombin aggregated, released about 80–90% 14C-serotinin and did not deaggregate spontaneously within 5 min from stimulation. Before ticlopidine, hirudin (5× the activity of thrombin) and PGE1 (10 μmol/1) plus chymotrypsin (10 U/ml) or plasmin (0.06 U/ml), added at the peak of platelet aggregation, caused slight or no platelet deaggregation. After ticlopidine, the extent of platelet deaggregation caused by the same inhibitors was significantly greater than before ticlopidine. The addition of ADP (10 μmol/1) to platelet suspensions 5 s after thrombin did not prevent the deaggregation of ticlopidine-treated platelets. Thus, ticlopidine facilitates the deaggregation of thrombin-induced human platelet aggregates, most probably because it inhibits the effects of ADP on platelets.

Accumulation of Macromolecular Particles in the Reticuloendothelial System (RES) Mediated by Platelet Aggregation and Disaggregation

1969 ◽  
Vol 22 (03) ◽  
pp. 496-507 ◽  
Author(s):  
W.G van Aken ◽  
J Vreeken
Keyword(s):  
Platelet Aggregation ◽  
Degradation Products ◽  
Reticuloendothelial System ◽  
Caproic Acid ◽  
Carbon Particles ◽  
Carbon Clearance ◽  
Aggregation And Disaggregation ◽  
Platelet Aggregates

SummaryCarbon particles cause platelet aggregation in vitro and in vivo. Prior studies established that substances which modify thrombocyte aggregation also influence the rate at which carbon is cleared from the blood.This study was performed in order to elucidate the mechanism by which the carbon-platelet aggregates specifically accumulate in the RES.Activation of fibrinolysis by urokinase or streptokinase reduced the carbon clearance rate, probably due to generated fibrinogen degradation products (FDP). Isolated FDP decreased the carbon clearance and caused disaggregation of platelets and particles in vitro. Inhibition of fibrinolysis by epsilon-amino-caproic acid (EACA), initially accelerated the disappearance of carbon and caused particle accumulation outside the RES, predominantly in the lungs. It is supposed that platelet aggregation and locally activated fibrinolysis act together in the clearance of particles. In the normal situation the RES with its well known low fibrinolytic activity, becomes the receptor of the particles.

Platelet Aggregation in Diabetes Mellitus and the Effect of Insulin in Vivo on Aggregation

1972 ◽  
Vol 27 (01) ◽  
pp. 114-120 ◽  
Author(s):  
A. A Hassanein ◽  
Th. A El-Garf ◽  
Z El-Baz
Keyword(s):  
Platelet Aggregation ◽  
Rapid Onset ◽  
Control Group ◽  
Diabetic Patients ◽  
Fasting State ◽  
Clotting Time ◽  
Cholesterol Levels ◽  
Platelet Disaggregation ◽  
Aggregation And Disaggregation

SummaryADP-induced platelet aggregation and calcium-induced platelet aggregation tests were studied in 14 diabetic patients in the fasting state and half an hour after an intravenous injection of 0.1 unit insulin/kg body weight. Platelet disaggregation was significantly diminished as compared to a normal control group, and their results were negatively correlated with the corresponding serum cholesterol levels. Insulin caused significant diminution in the ADP-induced platelet aggregation as a result of rapid onset of aggregation and disaggregation. There was also a significant increase in platelet disaggregation. In the calcium-induced platelet aggregation test, there was a significant shortening of the aggregation time, its duration, and the clotting time. The optical density fall due to platelet aggregation showed a significant increase. Insulin may have a role in correcting platelet disaggregation possibly through improvement in the intracellular enzymatic activity.

Effects of Bupranolol, a New β-Blocker, on Platelet Functions of Rabbit and Human in Vitro

1976 ◽  
Vol 36 (02) ◽  
pp. 376-387 ◽  
Author(s):  
Teruhiko Umetsu ◽  
Kazuko Sanai ◽  
Tadakatsu Kato
Keyword(s):  
Platelet Aggregation ◽  
Platelet Adhesion ◽  
Human Platelets ◽  
Rabbit Platelet ◽  
Rabbit Platelets ◽  
Β Blocker ◽  
Platelet Aggregates ◽  
Induced Aggregation ◽  
Platelet Functions

SummaryThe effects of bupranolol, a new β-blocker, on platelet functions were investigated in vitro in rabbits and humans as compared with propranolol, a well-known β-blocker. At first, the effect of adrenaline on ADP-induced rabbit platelet aggregation was studied because adrenaline alone induces little or no aggregation of rabbit platelets. Enhancement of ADP-induced rabbit platelet aggregation by adrenaline was confirmed, as previously reported by Sinakos and Caen (1967). In addition the degree of the enhancement was proved to be markedly affected by the concentration of ADP and to increase with decreasing concentration of ADP, although the maximum aggregation (percent) was decreased.Bupranolol and propranolol inhibited the (adrenaline-ADP-)induced aggregation of rabbit platelets, bupranolol being approximately 2.4–3.2 times as effective as propranolol. Bupranolol stimulated the disaggregation of platelet aggregates induced by a combination of adrenaline and ADP, but propranolol did not. Platelet adhesion in rabbit was also inhibited by the β-blockers and bupranolol was more active than propranolol. With human platelets, aggregation induced by adrenaline was inhibited by bupranolol about 2.8–3.3 times as effectively as propranolol.From these findings. We would suggest that bupranolol might be useful for prevention or treatment of thrombosis.

Systemic Effects of ADP-induced Platelet Aggregation and Their Modification by Aspirin and by Pyridinolcarbamate

1973 ◽  
Vol 30 (01) ◽  
pp. 178-190 ◽  
Author(s):  
Itsuro Kobayashi ◽  
Paul Didisheim
Keyword(s):  
Platelet Aggregation ◽  
Venous Pressure ◽  
Systemic Effects ◽  
Central Venous ◽  
Platelet Aggregates ◽  
Induced Changes ◽  
Second Wave ◽  
Carotid Arterial ◽  
Arterial Po2

SummaryADP, AMP, or ATP was injected rapidly intravenously in rats. ADP injection resulted in the f olio wing transient changes: a drop in platelet count, a rise in central venous pressure, a fall in carotid arterial PO2, bradycardia, arrhythmia, flutter-fibrillation, and arterial hypotension. AMP and ATP produced some of these same effects; but except for hypotension, their frequency and severity Avere much less than those following ADP.Prior intravenous administration of acetylsalicylic acid or pyridinolcarbamate, two inhibitors of the second wave of ADP-induced platelet aggregation in vitro, significantly reduced the frequency and severity of all the above ADP-induced changes except hypotension. These observations suggest that many of the changes (except hypotension) observed to follow ADP injection are produced by platelet aggregates which lodge transiently in various microcirculatory beds then rapidly disaggregate and recirculate.

Platelet Aggregation Induced in Vitro by Therapeutic Ultrasound

1977 ◽  
Vol 38 (03) ◽  
pp. 0640-0651 ◽  
Author(s):  
B. V Chater ◽  
A. R Williams
Keyword(s):  
Platelet Aggregation ◽  
Direct Action ◽  
Adenosine Diphosphate ◽  
Ultrasonic Cavitation ◽  
Related Phenomenon ◽  
Release Reaction ◽  
Physical Conditions ◽  
Platelet Aggregates ◽  
Active Substances

SummaryPlatelets were found to aggregate spontaneously when exposed to ultrasound generated by a commercial therapeutic device. At a given frequency, aggregation was found to be a dose-related phenomenon, increasing intensities of ultrasound inducing more extensive and more rapid aggregation. At any single intensity, the extent aggregation was increased as the frequency of the applied ultrasound was decreased (from 3.0 to 0.75 MHz).Ultrasound-induced platelet aggregation was found to be related to overall platelet sensitivity to adenosine diphosphate. More sensitive platelets were found to aggregate spontaneously at lower intensities of sound, and also the maximum extent of aggregation was found to be greater. Examination of ultrasound-induced platelet aggregates by electron microscopy demonstrated that the platelets had undergone the release reaction.The observation that haemoglobin was released from erythrocytes in whole blood irradiated under identical physical conditions suggests that the platelets are being distrupted by ultrasonic cavitation (violent gas/bubble oscillation).It is postulated that overall platelet aggregation is the result of two distinct effects. Firstly, the direct action of ultrasonic cavitation disrupts a small proportion of the platelet population, resulting in the liberation of active substances. These substances produce aggregation, both directly and indirectly by inducing the physiological release reaction in adjacent undamaged platelets.

The Ullrastructure of Platelet Participation in Hemostasis

1965 ◽  
Vol 13 (01) ◽  
pp. 065-083 ◽  
Author(s):  
Shirley A. Johnson ◽  
Ronaldo S. Balboa ◽  
Harlan J. Pederson ◽  
Monica Buckley
Keyword(s):  
Platelet Aggregation ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Guinea Pigs ◽  
Platelet Factor ◽  
Mesenteric Vessels ◽  
Platelet Aggregates ◽  
Electron Lucent

SummaryThe ultrastructure of platelet aggregation in vivo in response to bleeding brought about by transection of small mesenteric vessels in rats and guinea pigs has been studied. Platelets aggregate, degranulate and separating membranes disappear in parallel with fibrin appearance which is first seen at several loci after 30 seconds of bleeding. About 40 per cent of the electron opaque granules, some of which contain platelet factor 3 have disappeared after one minute of bleeding while the electron lucent granules increase by 70 per cent suggesting that some of them may be empty vesicles. Most of the platelet aggregates of the random type disappear leaving clumped red blood cells entrapped by a network of fibrin fibers which emanate from the remains of platelet aggregates of the rosette type to maintain hemostasis.

Functional Involvement of Thrombospondin in Platelet Aggregation Induced by Low Versus High Concentrations of Thrombin

1986 ◽  
Vol 55 (01) ◽  
pp. 136-142 ◽  
Author(s):  
K J Kao ◽  
David M Shaut ◽  
Paul A Klein
Keyword(s):  
Platelet Aggregation ◽  
Binding Sites ◽  
Inhibitory Effect ◽  
Activated Platelets ◽  
Low Concentrations ◽  
Platelet Binding ◽  
Functional Involvement ◽  
Thrombin Activation ◽  
Platelet Aggregates ◽  
High Concentrations

SummaryThrombospondin (TSP) is a major platelet secretory glycoprotein. Earlier studies of various investigators demonstrated that TSP is the endogenous platelet lectin and is responsible for the hemagglutinating activity expressed on formaldehyde-fixed thrombin-treated platelets. The direct effect of highly purified TSP on thrombin-induced platelet aggregation was studied. It was observed that aggregation of gel-filtered platelets induced by low concentrations of thrombin (≤0.05 U/ml) was progressively inhibited by increasing concentrations of exogenous TSP (≥60 μg/ml). However, inhibition of platelet aggregation by TSP was not observed when higher than 0.1 U/ml thrombin was used to activate platelets. To exclude the possibility that TSP inhibits platelet aggregation by affecting thrombin activation of platelets, three different approaches were utilized. First, by using a chromogenic substrate assay it was shown that TSP does not inhibit the proteolytic activity of thrombin. Second, thromboxane B2 synthesis by thrombin-stimulated platelets was not affected by exogenous TSP. Finally, electron microscopy of thrombin-induced platelet aggregates showed that platelets were activated by thrombin regardless of the presence or absence of exogenous TSP. The results indicate that high concentrations of exogenous TSP (≥60 μg/ml) directly interfere with interplatelet recognition among thrombin-activated platelets. This inhibitory effect of TSP can be neutralized by anti-TSP Fab. In addition, anti-TSP Fab directly inhibits platelet aggregation induced by a low (0.02 U/ml) but not by a high (0.1 U/ml) concentration of thrombin. In conclusion, our findings demonstrate that TSP is functionally important for platelet aggregation induced by low (≤0.05 U/ml) but not high (≥0.1 U/ml) concentrations of thrombin. High concentrations of exogenous TSP may univalently saturate all its platelet binding sites consequently interfering with TSP-crosslinking of thrombin-activated platelets.

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