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Träfflista för sökning "L773:2299 5684 OR L773:1734 1140 srt2:(2010-2014)"

Sökning: L773:2299 5684 OR L773:1734 1140 > (2010-2014)

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  • Hallbäck, Ida, et al. (författare)
  • In vitro effects of serotonin and noradrenaline reuptake inhibitors on human platelet adhesion and coagulation
  • 2012
  • Ingår i: Pharmacological Reports. - : Inst. of Pharmacology, Polish Acad. of Sciences. - 1734-1140. ; 64:4, s. 979-983
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Although several studies show that there is an increased risk of bleeding events during antidepressant treatment with selective serotonin reuptake inhibitors (SSRIs), few studies show direct effects in vitro of SSRIs on hemostasis. less thanbrgreater than less thanbrgreater thanMethods: This study was undertaken to investigate the effects on platelet adhesion and plasma coagulation (APTT and PT) of two common SSRIs, citalopram and sertraline, the selective noradrenaline reuptake inhibitor reboxetine, and the serotonin and noradrenaline reuptake inhibitor venlafaxine. less thanbrgreater than less thanbrgreater thanResults: None of the compounds affected plasma coagulation significantly but all compounds except for venlafaxine inhibited platelet adhesion by approximately 50% or more at the highest concentration (100 mu g/l, p andlt; 0.01). The potency of respective compound to inhibit platelet adhesion to both collagen and fibrinogen surfaces was in the following order; citalopram andgt; sertraline andgt; reboxetine. In contrast, venlafaxine caused a weak but statistically significant increased platelet adhesion to fibrinogen. less thanbrgreater than less thanbrgreater thanConclusion: This study showed that sertraline, citalopram and reboxetine direct and acutely decrease platelet adhesion to both collagen and fibrinogen in vitro. These results also indicate that increased risk for bleeding complications in antidepressant users may not only be explained by depletion of serotonin in platelets.
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  • Svensson, Anders I, 1969 (författare)
  • Flutamide treatment induces anxiolytic-like behavior in adult castrated rats
  • 2012
  • Ingår i: Pharmacological Reports. - 1734-1140. ; 64:2, s. 275-281
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: It has previously been speculated that the androgen receptor antagonist flutamide produces behavioral effects that are not mediated by androgen receptors. These earlier studies were performed in intact rodents and thus, flutamide may have interfered with endogenous testosterone produced by the testes. The main objective of the present study was to examine whether flutamide induces anxiolytic-like behavior in castrated rats. Methods: Male Wistar rats (8-9 weeks old) were castrated and thereafter, in the same operation, the rats received silastic capsules subcutaneously (sc)that were filled with dihydrotestosterone (DHT) or were left empty. Three weeks later, rats were cc administered tlutamide 50 mg/kg/day or vehicle for seven days. Four hours after the last injection, anxiolytic-like behavior was studied in a modified Vogel's drinking conflict model. In a separate experiment, shock threshold and drinking motivation were estimated. Results: Flutamide induced anxiolytic-like behavior in castrated rats irrespective of administration of DHT. Treatment with DHT alone did not induce a significant behavioral effect. Shock threshold and drinking motivation were not affected by flutamide and/or DHT treatment. Conclusions: This study demonstrates that flutamide induces anxiolytic-like behavior in a modified Vogel's conflict model in castrated rats, which indicates that flutamide has anxiolytic-like properties that are not dependent on testes-produced testosterone.
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