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1. |
Thrombocyte and Megathrombocyte Kinetics during Thrombocytosis Induced by Acute and Chronic Blood Loss and by Iron Deficiency Diet |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 121-135
S.K. Garg,
M. Weiner,
S. Karpatkin,
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摘要:
The mechanism of blood loss-induced thrombopoiesis was studied by measuring thrombocyte and megathrombocyte (young platelet) kinetics in guinea pigs made thrombocytotic by acute or chronic blood loss. The effect of an Fe-deficient diet was also examined. Acute and chronic blood loss raised the platelet count 1.2- and 1.4-fold, respectively Simultaneous replacement of Fe loss raised the platelet count 2.1- and 2.5-fold in acute and chronic blood loss, respectively. Paradoxically, an Fe-deficient diet also raised the platelet count 1.4-fold. Megathrombocyte number increased 1.4-fold more than the increase in platelet count for both acute and chronic blood loss. Simultaneous replacement of Fe produced an increase in megathrombocyte number which was 1.8- and 1.6-fold greater than the increase in platelet count for acute and chronic blood loss, respectively. Animals on an Fe-deficient diet did not raise their megathrombocyte number above their rise in platelet count. Thus, Fe is required for megathrombocyte production. A two-compartment system is postulated for the effect of Fe on thrombocytosis. (1) Fe inhibits the rise in platelet count above steady-state levels. (2) Fe is also required for maximum platelet production above steady-state levels via the production of megathrombocytes.The increment in megathrombocyte production following acute or chronic blood loss could account for one-quarter of thrombocyte production if one megathrombocyte gives rise to one thrombocyte. Alternatively, one megathrombocyte could give rise to four thrombocytes in the peripheral circulation. It is suggested that this latter mechanism may be important physiologically.
ISSN:1424-8832
DOI:10.1159/000213978
出版商:S. Karger AG
年代:1972
数据来源: Karger
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2. |
Heparin-Neutralizing Factor (Platelet Factor 4) from Human Blood Platelets and its Reactivity with Fibrinogen and Soluble Fibrin-Monomer Complexes |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 136-147
Rosmarie Käser-Glanzmann,
Milica Jakábová,
E.F. Lüscher,
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摘要:
The heparin-neutralizing factor (PF4) has been isolated from the supernatant of thrombin-treated, washed human blood platelets. The major part of the factor is present as a PF4-proteoglycan complex which can be dissociated at higher ionic strength. PF4 thus obtained is a basic protein of molecular weight 29,700. The carrier proteoglycan will recombíne with a maximum of 4 molecules of PF4, whereby dimerization of the resulting complex is observed. This is in contrast to the naturally occurring, released complex, which has a sedimentation constant which is rather compatible with the presence of monomeric material. Heparin displaces PF4 from its proteoglycan carrier; thereby a 1:1 heparin PF4 complex is formed. Contrary to preparations obtained by zinc precipitation, neither the PF4-carrier complex, nor purified PF4 obtained by dissociation at high ionic strength form insoluble complexes with fibrinogen or with complexes formed from fibrin-monomers and fibrinogen degradation products. Pretreatment of zinc-precipitated PF4 with EDTA abolishes its paracoagulating properties
ISSN:1424-8832
DOI:10.1159/000213979
出版商:S. Karger AG
年代:1972
数据来源: Karger
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3. |
Hyperactive Connective Tissue in Seven Patients with Recurrent Thrombotic Occlusions |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 148-155
Ulla Hedner,
Inga Marie Nilsson,
S.-E. Bergentz,
L. Cronberg,
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摘要:
A saline extract from the fascia of musculus rectus abdominis with increased capacity to aggregate the platelets in vitro was found in two uraemic patients with recurrent obstructive thrombosis frequently complicating the shunts used for haemodialysis, and in five patients with recurrent spontaneous deep venous thrombosis. None of these patients had any other disorder known to predispose to thrombosis. The increased capacity of the fascia extract to induce platelet aggregation may be due to a hitherto unknown cause of thrombosis, namely a defect in the collagen structure or in the subendothelial substances.
ISSN:1424-8832
DOI:10.1159/000213980
出版商:S. Karger AG
年代:1972
数据来源: Karger
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4. |
Aggregation of Human Platelets by Commercial Porcine and Bovine Fibrinogen Preparations |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 156-160
Charles D. Forbes,
Colin R.M. Prentice,
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摘要:
Commercial preparations of porcine and bovine fibrinogen which produce aggregation of human platelets have been shown to contain a high molecular weight compound. This material produces platelet aggregation and has procoagulant, chemical and antigenic identity with antihaemophilic factor.
ISSN:1424-8832
DOI:10.1159/000213981
出版商:S. Karger AG
年代:1972
数据来源: Karger
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5. |
Effect of Reserpine on14C-Serotonin Uptake by Human Platelet Populations |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 161-168
F. Rendu,
J.P. Caen,
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摘要:
The incorporation of 14C-5HT is inhibited by reserpine in heavy (young) human platelets, whereas it is enhanced in light (old) platelets. These findings are interpreted to mean that active uptake takes place in heavy (young) platelets, which probably have intact membranes rich in serotonin receptors, and a full content of ATP in storage granules, whereas passive diffusion is predominant in light (old) platelets.
ISSN:1424-8832
DOI:10.1159/000213982
出版商:S. Karger AG
年代:1972
数据来源: Karger
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6. |
Variation of the Proelastase/Elastase Ratio in Human Blood Platelet Populations |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 169-174
Y. Legrand,
G. Pignaud,
F. Fauvel,
J. Caen,
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摘要:
Human blood platelets have been separated into four populations according to their density, and the elastase activity measured in the presence and absence of trypsin in each of the four populations. Trypsin dependent elastolytic activity (proelastase) was higher in heavy (C and D) than in light (A and B) platelets, whereas trypsin independent elastolytic activity (elastase) was higher in light than in heavy platelets. The proelastase is presumably activated into fully active elastase as the platelet becomes lighter by an endogenous activating system.
ISSN:1424-8832
DOI:10.1159/000213983
出版商:S. Karger AG
年代:1972
数据来源: Karger
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7. |
Effects of Some Polyene Antibiotics on Human Platelets and their Function |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 175-190
P.M. van der Plas,
L. Kraan,
J. Stibbe,
H.C. Hemker,
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摘要:
(1) Polyenes aggregate platelets. The aggregation power diminishes in the following order: filipin > nystatin > etruscomycin∼pimaricin. (2) In the case of filipin, aggregation is probably caused by damage to platelets resulting in a release of platelet contents, which subsequent aggregates the remaining platelets. (3) Filipin-induced aggregation can be partially inhibited by adenosine and is Ca++ pimaricin. (6) The uptake of serotonin by platelets is diminshed by polyenes. Leakage of 86Rb from preloaded platelets increases upon addition of polyene
ISSN:1424-8832
DOI:10.1159/000213984
出版商:S. Karger AG
年代:1972
数据来源: Karger
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8. |
The Influence of the Polyene Filipin on the Extrinsic Pathway of Blood Coagulation |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 191-203
P.M. van der Plas,
G. van Es,
L. Kraan,
H.C. Hemker,
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摘要:
The inhibition by filipin in the extrinsic blood clotting system takes place at two sites: (1) at the interaction of factor VII, tissue thromboplastin and Ca++, and (2) at the prothrombinase level. Both formation and enzymatic activity of the prothrombinase are inhibited.The cholesterol content of the lipid that is used to form the prothrombinase complex determines the degree of inhibition by filipin. The inhibition increases the higher the sterol content. The adsorption of factors Xa and V onto lipid surface is enhanced by filipin. This increased adsorption does not lead to an increase in prothrombinase production.
ISSN:1424-8832
DOI:10.1159/000213985
出版商:S. Karger AG
年代:1972
数据来源: Karger
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9. |
Denaturation of Fibrinogen, the Protective Effect of Calcium |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 204-209
B. Ly,
H.C. Godal,
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摘要:
Small amounts of calcium provide protection of fibrinogen against moderate denaturation by heat or alkali. This protection remains despite dialysing the solution. These observations suggest that calcium might prevent denaturation of fibrinogen during preparation and storage.
ISSN:1424-8832
DOI:10.1159/000213986
出版商:S. Karger AG
年代:1972
数据来源: Karger
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10. |
Preparation of Human Fibrinogen Free of Plasminogen by Immunoadsorption |
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Pathophysiology of Haemostasis and Thrombosis,
Volume 1,
Issue 3-4,
1972,
Page 210-214
K.H. Luke,
J. Hirsh,
J. Bienenstock,
A. Zipursky,
M. Johnson,
K. Allman,
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摘要:
Human fibrinogen was purified free of plasminogen by a simple immunoadsorption technique using an insoluble polymer complex of an anti-plasminogen antiserum cross-linked by ethylchloroformate. The anti-plasminogen antiserum was prepared in guinea pigs by immunization with purified human plasminogen. The fibrinogen so purified was free of plasminogen as demonstrated by immunological and biological assays and did not show changes in clottability, thrombin clotting time and reactivity to plasmin, and is suitable as a reagent for plasmin and anti-plasmin assays for diagnostic purposes.
ISSN:1424-8832
DOI:10.1159/000213987
出版商:S. Karger AG
年代:1972
数据来源: Karger
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