摘要:

It appears that the binding of coagulation factor VIII to von Willebrand factor in plasma stabilizes the otherwise highly labile factor VIII. A mathematical model of factor VIII kinetics has been developed based upon this proposed effect of factor VIII binding. The model’s kinetic parameter values have been estimated by fitting the model to data available in the medical literature. The model gives accurate quantitative predictions of the elevated steady-state concentrations of factor VIII in clinical conditions associated with the acute phase reaction and in pregnancy, the decreased steady-state concentrations of factor VIII in females heterozygous for hemophilia, the decreased steady-state concentrations of factor VIII in patients with type 1 (heterozygous) and type 3 (homozygous) von Willebrand disease, and the variable half-life of factor VIII in factor replacement therapy for hemophilia and von Willebrand diseas

ISSN:1424-8832    

DOI:10.1159/000217222

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

In an attempt to characterise further the coagulopathy of childhood nephrotic syndrome, this study concentrates on simultaneous measurements of the natural anticoagulants [antithrombin III (ATIII), proteins C and S] and the fibrinolytic factors, tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI). The study groups consisted of 41 children (ages ranging from 2 to 14 years; median 7.1) in the relapse of nephrosis and 48 children (ages ranging from 3 to 14 years; median 7.6) in remission. The results obtained were compared with normal values obtained in healthy age- and sex-matched controls (n = 103). During relapse, there was a marked increase in the plasma level of fibrinogen, protein C, and protein S and reduced plasma ATIII level; tPA level was similar to control but PAI level exhibited a significant reduction. During remission, the protein C level either remained elevated or increased further, but some decreased. Protein S and plasma ATIII level normalised. The fibrinolytic activator tPA dropped slightly but the PAI level remained significantly below control levels. We conclude that in the relapse of childhood nephrosis, despite the existence of a significant prothrombotic tendency as featured by hyperfibrinogenaemia and markedly reduced ATIII level, the simultaneous elevation of the natural anticoagulant, protein C level and enhanced fibrinolysis that persist until the remission phase, seem to be major preventive mechanisms guarding nephrotic children against thromboembolic phenomena.

ISSN:1424-8832    

DOI:10.1159/000217223

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

To extend our previous in vitro data, we investigated the effects of cocaine on thromboxane A2 (TXA2) and prostacyclin (PGI2) production in vivo in the rat. To obtain the slight platelet activation that our in vitro experiments showed useful to highlight the effect of cocaine, we infused cocaine in rats in the presence of platelet-activating factors (circulation of blood through a perspex vascular device or by infusion of sodium arachidonate) and in various respiratory conditions. Experiments were conducted in rats breathing atmospheric air (nor-moxic conditions) and in rats breathing an oxygen-poor mixture (hypoxic conditions). In rats under hypoxic conditions cocaine invariably increased TXA2 plasma levels, whereas in normoxic conditions it increased TXA2 only in the presence of platelet-activating factors. Cocaine significantly increased PGI2 plasma levels in arachidonate-treated rats in hypoxic respiratory conditions; in normoxic conditions cocaine left PGI2 levels unchanged. These results support the hypothesis that in cocaine users who have concomitant pathological conditions able to activate platelets, such as atherosclerosis, coronary vasospasm or ischaemia, or both, cocaine may contribute to the onset of thrombotic phenomena by interfering with the prostaglandin system.

ISSN:1424-8832    

DOI:10.1159/000217224

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000217225

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000217226

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000217227

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000217228

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000217221

出版商:S. Karger AG    

年代:1996

数据来源: Karger