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Biomedical subjects

T Stoytchev

Publications and source records attributed to T Stoytchev.

51 records · Page 3Linked to original sources
PubMed1969

Combined effect of sodium maleate and some thiol compounds on mercury excretion and redistribution in rats.

1. (+)-Penicillamine in a dose of 193 mumoles/kg given subcutaneously twice a day on the sixth and seventh days after the administration of 100 mug mercury increased the urinary excretion of rats more than the equimolar dose of N-acetyl-(+)-penicillamine but less than 2,3-dimercaptopropanol 48.3 mumoles/kg.2. Sodium maleate in a dose of 156 mumoles/kg given on the sixth and seventh days after the mercury did not influence mercury excretion or redistribution. Sodium maleate in the same dose increased considerably the effect of (+)-penicillamine on the urinary excretion and redistribution of mercury. It increased the effect of N-acetyl-(+)-penicillamine only slightly. There was a tendency to decrease the effect of 2,3-dimercaptopropanol.3. All the complexing agents decreased the kidney content of mercury and increased the liver and blood concentration of mercury. These changes were highest with 2,3-dimercaptopropanol. The combination of sodium maleate with (+)-pencillamine caused higher mercury excretion and lower kidney content but a smaller increase in the liver and blood mercury contents than 2,3-dimercaptopropanol.

Animals↗
PubMedDate not supplied

Influence of rifampicin on the toxicity and the analgesic effect of acetaminophen.

The influence of rifampicin on the toxicity, analgesic effect and pharmacokinetics of acetaminophen was studied in male albino mice. Repeated administration of rifampicin (50 mg/kg i.p. daily for 6 days) shortened hexobarbital sleeping time and increased liver weight, microsomal cytochrome P-450 and heme contents, NADPH-cytochrome c reductase and ethylmorphine-N-demethylase activities. Aniline hydroxylase activity was decreased and glucuronidation of p-nitrophenol was unaffected. Rifampicin pretreatment changed neither the LD50 of acetaminophen nor the hepatic glutathione level nor the glutathione depletion provoked by the toxic dose of acetaminophen (737 mg/kg p.o.). This suggests that rifampicin has no influence on the amount of acetaminophen toxic metabolites formed in the liver. Rifampicin decreased the acetaminophen analgesic effect in mice. Rifampicin decreased the Cmax, the half-time, the MRT and the AUC of acetaminophen and accelerated its clearance. The plasma concentration of acetaminophen glucuronide and acetaminophen sulfate was increased. It is assumed that the most probable mechanism by which rifampicin decreases acetaminophen analgesia is the accelerated acetaminophen elimination.

Acetaminophen↗
PubMedDate not supplied

Effects of potassium ethylxanthogenate and 2,3-dimercaptopropane sulphonate sodium on the pentobarbital pharmacokinetics and metabolism in male mice.

The effects of potassium ethylxanthogenate (PEX) and 2,3-Dimercaptopropane sulphonate sodium (Unithiol) on the pentobarbital (40 mg/kg, body weight i.v.) (PB) sleeping time, pharmacokinetics, and metabolism, were studied in comparative experiments on male albino mice. It was established that the pretreatment of animals with PEX (80 mg/kg of body weight s.c.) potentiated the PB sleeping time. Unithiol in an equimolar dose (105.2 mg/kg of body weight s.c.) had no effect. The pharmacokinetics of PB could be fitted to be a biexponential equation of the type Cp(t) = A.e-alpha t + B.e-beta t. PEX caused an almost two-fold decrease in the elimination rate constant of plasma PB, which led to a higher half-time and a lower total clearance compared with the controls. The curve for the plasma PB metabolites in the PEX-pretreated mice was significantly lower than of the controls. A higher PB level and decreased rate of elimination in PEX-pretreated animals was observed also in the: liver, lungs, kidney, and brain. A conclusion was drawn that the potentiating effect of PEX on the PB sleeping time is mainly due to inhibition of PB liver metabolism. It was suggested that the differences in the biological effects of the two thiol compounds are due to the differences in their chemical structures: PEX possesses a C = S group but Unithiol lacks this group.

Animals↗
PubMedDate not supplied

Induction of cytochrome P-450 isozymes upon repeated administration of nifedipine.

In experiments on male Wistar rats it has been found that nifedipine administration at a dose of 10 mg/kg body weight i.p. daily for 20 days did not significantly increase the total amount of cytochrome P-450 but markedly increased the 7 alpha-, 16 beta- and 6 beta-hydroxylation of androstenedione in liver microsomes, suggesting the induction of cytochromes P-450IIA1, P-450IIB1, and P-450IIIA1, respectively. The induction of cytochrome P-450IIIB1 was also confirmed immunochemically with polyclonal antibodies against cytochrome P-450IIB1/B2.

Animals↗
PubMedDate not supplied

Interaction of dexamethasone with acetylsalicylic acid in mice.

The effect of acetylsalicylic acid (ASA, 160 mg/kg b.wt.) and dexamethasone (DEX, 15 mg/kg b.wt.) on ASA antinociception and toxicity when administered orally alone or in combination for 4 consecutive days was studied in male albino mice. ASA antinociception decreased after repeated ASA administration. Bleeding time was prolonged and the intestinal ASA esterase activity was increased, which was probably related to the increased ASA general toxicity in ASA-treated animals. There were no changes in the blood alkaline content, in the ulcerogenic or hepatotoxic effect of ASA, nor in the hepatic monooxygenase activity (ethylmorphine N-demethylase and aniline hydroxylase and the cytochrome P450 and b-5 content). DEX administered alone exerted a significant antinociceptive effect, increased both acute ASA toxicity and aniline hydroxylase activity and decreased body growth. However, DEX did not change the bleeding time, the alkaline blood content nor the intestinal esterase activity. The combination of ASA and DEX did not increase the ASA antinociceptive effect nor the general and specific toxicity of ASA. DEX in combination even abolished the effect of ASA on intestinal ASA esterase and on bleeding time. DEX also increased the hepatic cytochrome P450 content and did not change the ulcerogenic effect of ASA nor the alkaline blood content.

Administration, Oral↗