Search PubMed⌕ Search

Biomedical subjects

J Vermylen

Publications and source records attributed to J Vermylen.

At least 307 records · Page 17Linked to original sources
PubMed1975

Dissociation of clot retraction from platelet granule fusion and degranulation: an ultrastructural study of Reptilase-human platelet-rich plasma clots.

Human platelet-rich plasma clots, formed with Reptilase, do not retract. Electron microscopy of such a clot reveals platelets of normal shape and ultrastructural features surrounded by fibrin. When ADP is added before Reptilase, the clot strongly retracts. A sequential ultrastructural study of this process shows that, before visible fibrin formation, the platelets form small clusters and show shape change, granule centralization and pseudopod formation. Upon immobilization of the platelets by fibrin, the pseudopods develop into large cytoplasmatic protrusions, which allow cell contact. During the retraction process, the platelet granules remain intact; some granule fusion only becomes apparent in fully retracted clots. When Thrombofax is added to platelet-rich plasma before Reptilase, the clots formed also retract. With this aggregation inducer, granule fusion occurs earlier and in more platelets. Platelet pseudopod enlargement and fibrin concentration around the platelet mass are similar to that in ADP-treated samples. Inhibitors of granule fusion and secretion (suprofen, indomethacin) do not modify ADP-Reptilase nor Thrombofax-Reptilase clot retraction but reduce the incidence of granule fusion in Thrombofax-Reptilase clots. Retraction of Thrombofax-Reptilase clots is unaffected by concentrations of apyrase which completely block ADP-Reptilase clot retraction. Prostaglandin E1, papaverine and amitryptiline inhibit both ADP-and Thrombofax-Reptilase clot retraction, platelet pseudopod formation and cell-to-cell adhesion. These findings suggest that interaction of fibrin with the mass of fused granules (granulomere) or platelet secretion are not responsible for clot retraction. Rather, contraction around adhesion sites formed by cytoplasmic protrusions from adjacent platelets would seem to be involved.

Adenosine Diphosphate↗
PubMed1975

Activated reptilase clot retraction of dog platelet-rich plasma: differences with human platelet-rich plasma.

The retraction of dog platelet-rich plasma (PRP) clotted with Reptilase in the presence of inducers and inhibitors of the platelet adhesion-aggregation reaction was studied. In contrast to human cells, dog platelets fail to support retraction in an ADP-Reptilase system. With Thrombofax as aggregation inducer, slight (without additional CaCl2-MgCl2) to moderate (with additional CaCl2-MgCl2) retraction occurs. In contrast to human samples, such retraction is inhibited by platelet release inhibitors. Electron-microscopic examinations show that Thrombofax, but not ADP, induces the formation of large cytoplasmic protrusions from dog platelets. Such formation is inhibited by release-inhibitors. The results of the study support the concept that platelet pseudopod formation, rather than the release reaction, is a prerequisite for clot retraction.

Adenosine Diphosphate↗
PubMed1975

Effects of suprofen, an inhibitor of prostaglandin biosynthesis, on platelet function, plasma coagulation and fibrinolysis. I. In vitro experiments.

?The effects of suprofen, an inhibitor of prostaglandin biosynthesis, on human platelet function, fibrinolysis, proteolysis and coagulation in vitro were compared to those of reference compounds. Platelet aggregation induced by collagen, adrenaline and arachidonic acid was inhibited by suprofen depending on its concentration. Suprofen and indomethacin proved to have an equally inhibitory effect on platelet aggregation induced by collagen. Thrombin-induced aggregation was more inhibited by suprofen than by indomethacin. While the primary wave of A.D.P.-induced aggregation remained unchanged, the rate of disaggregation was enhanced by both compounds. Experiments on platelet factor-4 and 14C-serotonin release showed that suprofen and indomethacin reduced the platelet release reaction. Based upon results from experiments on synergism of suprofen with other compounds, on inhibition of arachidonic acid-induced platelet reactions and of prostaglandin E2-release, it is suggested that suprofen by inhibiting the prostaglandin biosynthesis in platelets also inhibits the platelet release reaction. In contrast to indomethacin and flufenamic acid, suprofen did not affect fibrinolysis or thrombin clotting activity. Tryptic proteolysis of albumin, however, was reduced by suprofen in a concentration-dependent and a substrate-competitive way. Tryptic decompisition of a synthetic substrate, on the other hand, was not reduced by either suprofen, indomethacin or flufenamic acid. These findings suggest that the observed reduction of albumin proteolysis by suprofen is related to an effect on the protein substrate rather than on the proteolytic enzyme itself.

Adenosine Diphosphate↗
PubMed1975

Effects of suprofen, an inhibitor of prostaglandin biosynthesis, on platelet function, plasma coagulation and fibrinolysis II. In vivo experiments.

Suprofen, an inhibitor of prostaglandin biosynthesis, was found to affect certain aspects of platelet function after in vivo administration in various species. In guinea-pigs, platelet aggregation induced by collagen and Thrombofax, and secondary A.D.P. aggregation were reduced in a dose-dependent way by suprofen (single oral administration) from 0.08 mg/kg on. In dogs, the effect of a single oral dose of 2.5 mg/kg of suprofen on collagen-induced aggregation started 30 min after administration, lasted for at least 8 h and had disappeared after 24 h. Plasma coagulation parameters were not affected by the compound in this species. In rats, suprofen prolonged tail bleeding times, but did not modify fibrinolysis, platelet adhesion to glass beads or plasma coagulation. Sub-chronic administration of comparatively high doses of the compound resulted in potentiation of the anti-coagulant effect of warfarin in this species.

Adenosine Diphosphate↗
PubMed1975

Physical and chemical properties of normal and haemophilic factor VIII.

This review summarizes the physical and chemical properties of normal factor VIII (antihaemophilic factor). Special attention is given to the different subunits of this molecule, obtained after dissociation by beta-mercaptoethanol, high or low ionic strength. Present points of controversy are outlined. A description is given of the role of factor VIII in coagulation, as it is presently understood. The studies of the physical and chemical properties of haemophilic factor VIII also are reviewed; the molecular defect of haemophilic factor VIII remains to be identified.

Binding Sites↗
PubMed1974

Indomethacin and platelet aggregation in chronic glomerulonephritis: existence of non-responders.

Indomethacin given to adults with glomerulonephritis usually reduces their urinary excretion of protein and fibrinogen/fibrin-related (F.R.) antigen. Nevertheless, non-responders exist. Platelet aggregation is significantly more strongly inhibited by indomethacin in good responders than in nonresponders. This supports the hypothesis that the reduction of urinary excretion of F.R. antigen during indomethacin administration is related, at least in part, to inhibition of intrarenal platelet aggregation and of the subsequent fibrin deposition.

Adolescent↗
PubMed1974

The antigenic determinant of fibrin(ogen) measured with agglutination inhibition immunoassays.

Agglutination inhibition immunoassays using antifibrinogen antiserum measure an antigenic determinant of fibrinogen which is located on the fragment D parts of this molecule. This antigenic determinant of fragment D, in contrast to others, does not form an immune precipitate with antifibrinogen antiserum. Upon very extensive hydrolysis by plasmin, this antigenic determinant has a reduced affinity for its antibody.

Blood Protein Electrophoresis↗