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Träfflista för sökning "L773:0957 5235 srt2:(1992-1994)"

Sökning: L773:0957 5235 > (1992-1994)

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1.
  • Casslén, B, et al. (författare)
  • Plasminogen activators in the human endometrium, cellular origin and hormonal regulation.
  • 1992
  • Ingår i: Blood Coagulation and Fibrinolysis. - 0957-5235 .- 1473-5733. ; 3:2, s. 133-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Endometrial tissue explants in culture were found to release urokinase-type plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA). In order to identify their cellular origin and possible hormonal regulation, enriched cultures of glandular epithelial cells and stromal cells were prepared from fresh endometrium, and the cultures treated with hormones. Both epithelial and stromal cell cultures were found to secrete u-PA and t-PA. Treatment of epithelial cell cultures with oestradiol, progesterone and DH-testosterone had no effect on the secretion of t-PA or u-PA. In stromal cell cultures, on the other hand, the secretion of u-PA was significantly reduced after treatment with progesterone, whereas oestradiol and DH-testosterone had no effect. This reduction of u-PA antigen in the tissue culture medium did not result from a reduction of the relative level of u-PA mRNA in the cells, suggesting that the synthesis of u-PA was not reduced. Alternatively, an increased clearance of u-PA by the cells from the medium may explain the reduction. This in vitro observation probably reflects the in vivo reduction of u-PA in endometrial secretion during the secretory phase.
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2.
  • Henriksson, Anders E., et al. (författare)
  • Time course of clotting and fibrinolytic markers in acute upper gastrointestinal bleeding : relation to diagnosis and blood transfusion treatment.
  • 1993
  • Ingår i: Blood Coagulation and Fibrinolysis. - 0957-5235 .- 1473-5733. ; 4:6, s. 877-80
  • Tidskriftsartikel (refereegranskat)abstract
    • One hundred consecutive patients with acute upper gastrointestinal bleeding were investigated. Blood coagulation and fibrinolytic activity were monitored by levels of plasma thrombin-antithrombin III (TAT) complex and plasmin-alpha 2-antiplasmin (PAP) complex in samples obtained from patients at admission with haematemesis and/or melana and in samples obtained from patients the first day after admission. Blood was transfused according to a restrictive policy. Median plasma TAT complex was significantly elevated both at admission and on the first day after admission compared with a reference group. Plasma PAP complex levels were normal at admission but decreased on the first day after admission. This decrease was independent of blood transfusion. The results indicate hypercoagulability at admission among patients with upper gastrointestinal haemorrhage reinforced by the development of a hypofibrinolytic state during the first day after admission. Restricted blood transfusion was not associated with any detectable change in blood coagulation or fibrinolysis in these patients.
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3.
  • Holst, J., et al. (författare)
  • Protamine neutralization of intravenous and subcutaneous low-molecular-weight heparin (tinzaparin, Logiparin(TM)). An experimental investigation in healthy volunteers
  • 1994
  • Ingår i: Blood Coagulation and Fibrinolysis. - 0957-5235. ; 5:5, s. 795-803
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of the present study was to investigate whether tinzaparin sodium (a low-molecular-weight heparin (LMWH)) was fully and permanently neutralized in vivo in man by protamine sulphate (PS) after intravenous (i.v.) or subcutaneous (s.c.) injection. Fifty healthy adults equally divided in five age- and sex-matched groups were included. The groups received 50 IU unfractionated heparin (UH)/kg body weight (b.w.) i.v., 50 anti-factor Xa (anti-Xa) IU tinzaparin/kg b.w. i.v., 75 anti-Xa IU tinzaparin/kg b.w. s.c., 175 anti-Xa IU tinzaparin/kg b.w. s.c., or 1 ml of saline s.c. PS was given as a 10 min infusion in a dose of 1 mg/100 IU of heparin in the four first groups while 0.5 mg PS/kg b.w. was given in the placebo group. In the i.v. groups PS was administered 45 min after the heparin injection, and in the s.c. groups 180 min post-heparin injection. In the UH group PS fully and permanently neutralized all three activities. In the i.v. tinzaparin group PS reversed 80% of the anti-Xa activity, while the anti-IIa and aPTT activities were fully reversed. A slight, but statistically significant, increase in anti-Xa and anti-Ila activities were seen following i.v. tinzaparin. In the s.c. groups 60-65% of the observed peak anti-Xa activity was neutralized, anti-IIa was almost completely reversed, and aPTT returned nearly to baseline values. A gradual return of the anti-Xa activity (65-75%), anti-IIa activity (55%) and aPTT activity (35-45%) was seen in the s.c. groups 3 h after reversal compared with the observed peak values. A continuous absorption of tinzaparin from the s.c. depot is presumably the cause of the returned activity. PS caused an 8-27% transient drop in the platelet count in all groups. This study confirms that the anti-Xa activity following i.v. and s.c. administration of tinzaparin (a LMWH) is only partially neutralizable by protamine. This is not due to insufficient dosages of the antidote, as an excess of protamine could be demonstrated ex vivo immediately after the protamine infusion. The present results suggest that protamine neutralization of tinzaparin given s.c. should be obtained with intermittent injections or continuous infusion.
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