P Cieslar

Charles University

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IŠ

Ivan Špıčka

Charles University

F Heřmanský

Czech Academy of Sciences, Institute of Experimental Medicine

P Klener

Charles University

O Matoušová

Charles University

B Friedmann

IQVIA (United Kingdom)

E Beńesová

University of Chemistry and Technology, Prague

J Sálková

Charles University

M Chrz

AeskuLab (Czechia)

Bohumír Procházka

National Institute of Public Health

J. Greenberg

Ministry of Agriculture and Rural Development

Cooperative Institutions

Charles University

General University Hospital in Prague

Institute of Haematology and Blood Transfusion

Iscare I.V.F

McMaster University

University of Toronto

Instytut Hematologii i Transfuzjologi

Institute of Clinical and Experimental Medicine

Masaryk University

University Hospital Kralovske Vinohrady

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Separation of Degranulated Platelets from Normal Platelets

Thrombosis and Haemostasis (1977)

P Cieslar J. Greenberg MA Packham R L Kinlough-Rathbone J. F. Mustard

Platelets degranulated by thrombin (TDP) can be recovered, are effective in hemostasis and survive normally upon infusion into rabbits. Two approaches to determine whether platelets have been degranulated in vivo are: (1) measurement of circulating released materials; (2) detection of circulating degranulated platelets. We have used arabino-galactan (Stractan II) density gradient centrifugation to separate normal and degranulated platelets. The following distribution was obtained with washed rabbit platelets. The serotonin, PF4 and adenine nucleotide contents of the TDP were less than those of normal platelets and the TDP in fraction I had the lowest amounts. When TDP were labeled with 51cr and mixed with equal numbers of normal platelets, 85% of the platelets in fraction I were found to be TDP. 51Cr-TDP were injected into normal rabbits and reharvested after 18 hours. The greatest proportion of TDP was isolated in fraction I. Thus this method may make it possible to separate platelets that have lost their granule contents during participation in reversible thrombus formation in vivo. (* Visiting Fellow from the Faculty of Medicine, Charles University, Prague, Czechoslovakia.)

Ristocetin

Blood Platelet Disorders

Platelet adhesiveness

Thrombopoiesis

10.1055/s-0039-1682656

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Citations (3)

[Holter monitoring of patients treated with cytostatic agents].

PubMed (1989)

M. Kozàkovà E Beńesová P Cieslar J Sálková

After cytostatic treatment severe arrhythmias, the development of angina pectoris and even the development of acute myocardial infarction and sudden death were observed. Therefore we made in 42 patients with malignant haematological disease treated with cytostatics 96 Holter monitorings of the electrocardiographic signal. The monitoring was made during the administration of cytostatics as well as during the time interval between the administration of combinations of cytostatics. In both instances (during the administration and during the interval between administration) we recorded a surprisingly high, mean all-day as well as maximal, heart rate. In the group monitored during administration of chemotherapeutic drugs we observed 5-8 hours after administration of cytostatics serious ventricular arrhythmias [incl. ventricular tachycardia], denivelization of the ST segment, paroxysms of supraventricular tachycardia. In the group monitored during the interval between administration of cytostatics the sick-sinus syndrome was recorded, as well as a passive nodal rhythm, disorders of the intraventricular conduction. The described changes are explained by the release of vasoactive substances after administration of cytostatics, by a change of the transmembrane calcium transport leading to an increased excitability of the heart muscle and possibly to coronary spasms and direct irreversible damage of the conduction system.

Sudden Death

Sick sinus syndrome

Supraventricular arrhythmia

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Citations (1)

[Treatment of chronic proliferative glomerulonephritis using acetylsalicylic acid and dipyridamole].

PubMed (1989)

Knotková I Petrů Karel Němeček P Cieslar Jan Peleška

Fourteen patients with chronic proliferative glomerulonephritis were given for the period of one year 400 mg acetylsalicylic acid and 225 mg dipyridamole per day. During this treatment the thrombocyte aggregation became normal, however, the mean reduction of antiheparin plasma activity was not statistically significant. Normal synthesis of renal prostacyclin declined significantly as a result of treatment, while the renal thromboxane A2 synthesis remained normal even during treatment. Treatment did not influence proteinuria. The mean annual decline of glomerular filtration was greater during the investigation period than the mean annual decline in previous years, the difference was, however, only at the borderline of statistical significance. The authors did not prove a favourable effect of this treatment in patients with chronic proliferative glomerulonephritis.

Dipyridamole

Thromboxane B2

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Citations (2)

Oxidative stress and platelet function in multiple myeloma and renal insufficiency

Thrombosis Research (2002)

P Cieslar L. Mášová Tomáš Scheiner Jitka Ryšavá Petra Křı́žová

Malondialdehyde

Platelet adhesiveness

10.1016/s0049-3848(02)00003-8

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Citations (10)

Hereditary thrombocytopathies with abnormal release reaction (author's transl).

PubMed (1976)

F Heřmanský P Cieslar

The authors have examined 8 cases with Hermansky-Pudlak syndrome in whom besides the usual abnormalities of abnormal aggregation with collagen, absence of second wave of aggregation, reduction of the 5-HT uptake, presence of 5-HIAA in the platelets, two new abnormalities are described: the presence of a large amount of an unidentified metabolite after 5-HT incorporation which differs from 5-HT and 5 hydroxytryptophol and an abnormal incorporation of labelled glycerol in the triglycerides. Correlation between abnormal lipid metabolism and defective 5-HT incorporation is discussed.

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[Myeloma in a 28-year old man (author's transl)].

PubMed (1981)

M Englis P Cieslar F Heřmanský

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Investigation of In Vivo Factors that May Influence Platelet Survival and Density

Thrombosis and Haemostasis (1979)

Marian A. Packham J. F. Mustard M A Guccione P.D. Winocour H M Groves

Platelet survival CPS) is shortened in a number of conditions but the mechanisms responsible are unclear. In rabbits, removal of the aortic endothelium or injury of the neointima does not shorten PS. However, induction of thrombi in rabbit aortae with Indwelling cannulae (IDC) shortens FS (IDC 37.0 hr, control 79.6 hr), and Increases the proportion of platelets in the lightest fraction upon straetan density gradient centrifugation. Therefore we examined the effect of agents to which platelets may be exposed during thromboembolism (ADP, thrombin, plasmin) on PS and platelet density. ADP treatnent of washed rabbit platelets did not alter their survival but did increase the proportion in the lightest fraction. Treatment of platelets with thrombin did not shorten PS but increased the proportion in the lightest fraction. Treatment with plasmin in vitro shortened PS (plasmin, 57.6 ± 6.0 hr, control 80.2 ± 4,2 hr) and increased the proportion in the lightest fraction. Thus changes in platelet density are not necessarily associated with changes in PS. Of the factors investigated that are known to be involved in thromboembolism, only plasmin shortened PS. This may be due to its ability to alter major platelet membrane glycoproteins(principally glycoproteins I and II of rabbit platelets).

Neointima

10.1055/s-0039-1687309

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Citations (9)

[Blood platelet function in chronic myeloid-type diseases. I. Myeloproliferative diseases].

PubMed (1987)

P Cieslar O Matoušová

Myeloproliferative Disorders

Chronic myeloid leukaemia

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[Anemia in chronic diseases. Brief review].

PubMed (1984)

B Friedmann E Beńesová P Cieslar J Sálková

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[Hemostasis disorders in monoclonal gammopathies].

PubMed (1991)

Ivan Špıčka P Cieslar Dyr Je O Matoušová

The authors investigated haemostatic parameters of 43 patients with monoclonal gammapathy with principal diagnosis of multiple myeloma (MM-35), non-Hodgkin's lymphoma (NHL-3), M. Waldenström (3) and monoclonal gammapathy of undetermined significance (MGUS-2). Primary haemostasis defect was found in 24 patients. With the exception of 2 thrombocytopenic patients, the defect of aggregation, procoagulant activity and retraction is supposed to be caused by paraprotein. The examination of the 14C 5-HT release and TX B2 synthesis in thrombocytes showed, that platelet activation is unaffected and the paraprotein interferes with interactions of thrombocytes or with coagulation system. In plasma coagulation system explicit abnormalities were found only in thrombin time in 12 patients. The more detailed examination disclosed, that the defect resulted from paraprotein interference with fibrin monomer polymerisation. The thrombin proteolytic activity remained unaffected. In 3 patients shortened euglobulin lysis time was observed. Laboratory haemostasis defect was found in 26 patients (60%), however, the bleeding symptoms manifested in 5 cases (11%) only. The analysis of study results showed, that the most important abnormalities leading to overt bleeding are thrombocytopenia or combined haemostasis defect. Isolated laboratory defects remained silent in most cases.

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Citations (5)