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hydroxytoluene/versterkte bloedingsneiging

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LidwoordKlinische proevenOctrooien
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Preventive effects of phylloquinone on hemorrhagic death induced by butylated hydroxytoluene in male rats.

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The effects of vitamin K on hemorrhagic death induced by dietary butylated hydroxytoluene (BHT) were studied. Male Sprague-Dawley rats were given BHT or two phenolic antioxidants (2,4,6-tri-tert-butylphenol and 2,5-di-tert-butylhydroquinone) in combination with a 24% casein basal diet. The levels of
Groups of ten male Slc:ddY mice were fed a purified diet containing butylated hydroxytoluene (BHT) at levels of 0, 1.35, 1.75, 2.28, 2.96, 3.85 or 5.00%. They were kept in cages with soft-wood chips as bedding for 30 days. Groups of five Slc:ddY male mice were kept in cages with stainless-steel
Measurements of platelet-particle concentration, platelet haematocrit and mean platelet volume showed no significant differences between control rats and rats given 1.2% butylated hydroxytoluene (BHT) in the diet for 1 wk, but the platelet distribution width was significantly smaller in the rats fed
Single oral doses of the haemorrhagic antioxidant 2,4,6-tri-t-butylphenol (260 mg/kg) were well absorbed in the rat. Peak blood levels of this compound were reached in 15-60 min. The blood elimination half-lives were 18.2 min for the alpha-phase and 11.8 h for the slower beta-phase. Max. tissue

Haemorrhagic toxicosis in rats given butylated hydroxytoluene.

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Vascular permeability, platelet function, blood coagulation and fibrinolytic activity were examined in Sprague-Dawley male rats given 1.20% butylated hydroxytoluene (BHT) in the diet for 1 week. BHT significantly increased the leakage of Evans blue from blood into epididymus. BHT inhibited the

Species differences in the haemorrhagic response to butylated hydroxytoluene.

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Dose--response study of hemorrhagic death by dietary butylated hydroxytoluene (BHT) in male rats.

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Male Sprague-Dawley rats and male ICR mice, species respectively susceptible and resistant to the haemorrhagic effect of butylated hydroxytoluene (BHT), were administered BHT quinone methide (2,6-di-tert-butyl-4-methylene-2,5-cyclohexadienone) orally; 24 or 48 h later the plasma concentrations of

Hemorrhagic toxicity of d-alpha-tocopherol in the rat.

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When male Sprague-Dawley rats were administered d-alpha-tocopherol and butylated hydroxytoluene in the diet or intraperitoneally for 7 days, prolongations of prothrombin time and partial thromboplastin time were observed in those given both chemicals by both routes in a dose-dependent manner.

Some properties of rat platelet aggregation and effects of butylated hydroxytoluene, warfarin and aspirin.

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The platelet aggregation characteristics of male Sprague-Dawley (Jcl:SD) rats were investigated. Epinephrine, ristocetin, serotonin and platelet-activating factor were ineffective in rat platelets. Heparinized platelet-rich plasma (PRP) was more sensitive than citrated PRP to three aggregating
Male Sprague-Dawley rats were fed a diet containing 1.2% butylated hydroxytoluene (BHT) for 1-7 days, and blood coagulation factors II, VII, VIII, IX and X, and platelet aggregation were measured. The plasma concentrations of factors II, VII, IX and X were significantly reduced in a time-dependent

The dose-dependent effect of BHT (butylated hydroxytoluene) on vitamin K-dependent blood coagulation in rats.

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Earlier studies have reported a reduction of vitamin K-dependent blood clotting factor activity and incidence of haemorrhagic death in rats fed butylated hydroxytoluene (BHT); however, the vitamin K status of the animals used in these studies was claimed to be inadequate. The aim of the study

Lung hemorrhagic toxicity of butylated hydroxyanisole in the rat.

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Male Sprague-Dawley rats were injected intraperitoneally (i.p.) with butylated hydroxyanisole (BHA) at doses of 0, 1, 4, 16, 64, 256, 384, 576, 864, 1296 and 1944 mg/kg/day for 7 days. Deaths occurred in a dose- and time-dependent manner when BHA was given in amounts greater than 576 mg/kg. The LD50

Central adrenergic mechanisms in hemorrhage-induced vasopressin secretion.

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The effect of central administration of specific adrenergic agonists and antagonists on hemorrhage-induced vasopressin secretion was studied in conscious rats. The intracerebroventricular (icv) injection of the alpha 2-antagonist yohimbine, the alpha 1-antagonist corynanthine, or the beta-agonist
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