Lack of an Acute Effect of Pb2+ on Platelet Aggregation

1992 ◽  
Vol 68 (03) ◽  
pp. 373-373
Author(s):  
S Nesaratnam ◽  
S Bawa ◽  
M C Scrutton
Platelets ◽  
2009 ◽  
Vol 20 (8) ◽  
pp. 606-609 ◽  
Author(s):  
Kiran D. K. Ahuja ◽  
Murray J. Adams ◽  
Iain K. Robertson ◽  
Madeleine J. Ball

1979 ◽  
Author(s):  
S. Villa ◽  
A.E. Cavenaghi ◽  
G. de Gaetano

Suloctidil [1-(4-isopropyl-thiophenyl)-2-n-octylaminopropanol, Continental Pharma, Belgium] is a drug which inhibits platelet aggregation in human beings and possesses antiplatelet aggregation and antithrombotic properties in several animal models. In the present study, the acute effect of suloctidil on vascular prostacyclin activity was evaluated in rats.. Male CD rats (250-300 g) were given the drug (200-400 mg/kg b.w.) orally 1 h before testing. Prostacyclin activity was measured as the plotelet aggregation inhibitory potency of supernatant buffer following 4 min incubation with rings of either abdominal aorta or inferior vena cava. Treatment with suloctidil did not induce any significant modification of prostacyclin activity. In contrast, in vivo platelet aggregation induced by i.v. infusion of ADP (1 mg/kg) or collagen (2.6 mg/kg) was significantly (p < 0.001) inhibited. It is su.ggested that suloctidil may interfere with platelet function without affecting the potential antithrombotic activity of the vascular wall.


Author(s):  
W. H. Zucker ◽  
R. G. Mason

Platelet adhesion initiates platelet aggregation and is an important component of the hemostatic process. Since the development of a new form of collagen as a topical hemostatic agent is of both basic and clinical interest, an ultrastructural and hematologic study of the interaction of platelets with the microcrystalline collagen preparation was undertaken.In this study, whole blood anticoagulated with EDTA was used in order to inhibit aggregation and permit study of platelet adhesion to collagen as an isolated event. The microcrystalline collagen was prepared from bovine dermal corium; milling was with sharp blades. The preparation consists of partial hydrochloric acid amine collagen salts and retains much of the fibrillar morphology of native collagen.


2010 ◽  
Vol 24 (4) ◽  
pp. 249-252 ◽  
Author(s):  
Márk Molnár ◽  
Roland Boha ◽  
Balázs Czigler ◽  
Zsófia Anna Gaál

This review surveys relevant and recent data of the pertinent literature regarding the acute effect of alcohol on various kinds of memory processes with special emphasis on working memory. The characteristics of different types of long-term memory (LTM) and short-term memory (STM) processes are summarized with an attempt to relate these to various structures in the brain. LTM is typically impaired by chronic alcohol intake but according to some data a single dose of ethanol may have long lasting effects if administered at a critically important age. The most commonly seen deleterious acute effect of alcohol to STM appears following large doses of ethanol in conditions of “binge drinking” causing the “blackout” phenomenon. However, with the application of various techniques and well-structured behavioral paradigms it is possible to detect, albeit occasionally, subtle changes of cognitive processes even as a result of a low dose of alcohol. These data may be important for the consideration of legal consequences of low-dose ethanol intake in conditions such as driving, etc.


2014 ◽  
Author(s):  
Somrudee Saiyudthong ◽  
Sirinun Pongmayteegul ◽  
Udomsri Showpittapornchai ◽  
Pansiri Phansuwan-Pujito

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
M Dell'Agli ◽  
R Fagnani ◽  
G Galli ◽  
O Maschi ◽  
E de Fabiani ◽  
...  

1998 ◽  
Vol 79 (01) ◽  
pp. 211-216 ◽  
Author(s):  
Lysiane Hilbert ◽  
Claudine Mazurier ◽  
Christophe de Romeuf

SummaryType 2B of von Willebrand disease (vWD) refers to qualitative variants with increased affinity of von Willebrand factor (vWF) for platelet glycoprotein Ib (GPIb). All the mutations responsible for type 2B vWD have been located in the A1 domain of vWF. In this study, various recombinant von Willebrand factors (rvWF) reproducing four type 2B vWD missense mutations were compared to wild-type rvWF (WT-rvWF) for their spontaneous binding to platelets and their capacity to induce platelet activation and aggregation. Our data show that the multimeric pattern of each mutated rvWF is similar to that of WT-rvWF but the extent of spontaneous binding and the capacity to induce platelet activation and aggregation are more important for the R543Q and V553M mutations than for the L697V and A698V mutations. Both the binding of mutated rvWFs to platelets and platelet aggregation induced by type 2B rvWFs are inhibited by monoclonal anti-GPIb and anti-vWF antibodies, inhibitors of vWF binding to platelets in the presence of ristocetin, as well as by aurin tricarboxylic acid. On the other hand, EDTA and a monoclonal antibody directed against GPIIb/IIIa only inhibit platelet aggregation. Furthermore, the incubation of type 2B rvWFs with platelets, under stirring conditions, results in the decrease in high molecular weight vWF multimers in solution, the extent of which appears correlated with that of plasma vWF from type 2B vWD patients harboring the corresponding missense mutation. This study supports that the binding of different mutated type 2B vWFs onto platelet GPIb induces various degrees of platelet activation and aggregation and thus suggests that the phenotypic heterogeneity of type 2B vWD may be related to the nature and/or location of the causative point mutation.


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