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Biomedical subjects

W Volkert

Publications and source records attributed to W Volkert.

6 recordsLinked to original sources
PubMed1999

Rhodium-105 tetrathioether complexes: radiochemistry and initial biological evaluation.

105Rhodium(III) complexes with three different acyclic tetrathioether ligands containing pendant carboxylic acid groups have been synthesized and characterized. The complexes were evaluated for stability under physiological conditions and the most promising complexes were evaluated in vivo in normal mice. The primary route of clearance for these complexes was the renal/urinary system, consistent with the presence of pendant carboxylate groups. The results indicate that the cis-[Rh(III)Cl2(2,5,8,11-tetrathiadodecane-1,12-dicarboxylic acid)]+ complex shows the most promising in vivo characteristics on which to base a potential therapeutic radiopharmaceutical.

Animals↗
PubMed1983

A new Cd-115 leads to In-115m radionuclide generator.

A new column-type Cd-115 leads to In- 115m generator has been developed by adsorbing CdI4(-2) on an anion-exchange resin and eluting the In-115m with 0.05 M HCl. The In-115m yield of the prototype column is 90% in a volume of 3 ml, with Cd-115 breakthrough of less than 3 X 10(-4)%. Over thirty generators with up to 40 mCi of activity have been produced using components of a commercial Mo-99 leads to Tc-99m generator system; they behaved like the prototype. In-115m oxine prepared from these generators has been used to label canine platelets and to image an induced canine thrombus in vivo.

Animals↗
PubMed1980

Complexing of Tc-99m with cyclam: concise communication.

The macrocyclic amine, cyclam, has been found to be an efficient complexing agent for Tc-99m. Complexes can be formed in yields of higher than 95% at pH 11 in 10(-3) M cyclam using 5 x 10(-6) M SnC4H4O6 as a reducing agent. The complex is positively charged and is stable in air. It is not decomposed by dilution, by 0.05 M NaOH, or 0.05 M H2O2, but does show slight decomposition in 0.05 M HCl. In unanesthetized mice the complex is cleared rapidly from the blood by the kidneys and liver. Preliminary studies show that derivatives of cyclam also complex Tc-99m.

Animals↗
PubMed1978

[The influence of a combination of clonidine and acetylandromedol on blood pressure and central sympathetic tone of the cat (author's transl)].

The effects of acetylandromedol alone and in combination with 2-(2,6-dichlorophenolamino)-2-imidazoline hydrochloride (clonidine) on the arterial blood pressure and the preganglionic discharges of the cervical sympathetic and phrenic nerves were studied in 36 anaesthetized cats. At a dosage of 10--40 micrograms/kg i.v. acetylandromedol produced a fall of blood pressure and an increase of the central nervous sympathetic activity. Both effects lasted longer than 1 h. The combination of 40 micrograms acetylandromedol/kg with 15 micrograms clonidine/kg i.v. caused a decrease of the sympathetic activity. A depression of the respiratory centres was not observed. 10 micrograms acetylandromedol/kg in combination with 15 micrograms clonidine/kg produced a significantly more pronounced hypotensive action than the single application of 20 micrograms acetylandromedol/kg or 30--120 micrograms clonidine/kg.

Action Potentials↗
PubMed1977

[Studies on the mechanism of action of clonidine (author's transl)].

The effects of 3.7-120 microgram 2-(2,6-dichloro-anilino)-2-imidazoline (clonidine, Catapresan)/kg i.v. on the arterial blood pressure and the central nervous activities of sympathetic and phrenic nerves were studied in 42 anaesthetized cats which had been relaxed and artificially respirated. At the dosage 3.7-30 microgram/kg clonidine produced a moderate fall of blood pressure and a more distinct sympathetic inhibitory effect. At a dosage of 60-120 microgram/kg an increase of the hypotensive action was not observed whereas the central nervous inhibition increased with the dosage. The activity of the respiratory centre remained constant. The pressor effects as well as the sympathetic stimulation effects of nicotine, nicetamide or asphyxia were reduced by the treatment with clonidine. At a dosage of 3.7-30 microgram clonidine/kg, i.e. including the 6fold therapeutic dosage, the inhibition of the evoked sympathetic activity was, however, considerably weaker than the inhibition of the sympathetic activity at rest. Therefore clonidine at a therapeutic dosage probably causes an activation of the central part of the pressor-receptor reflexes and as a result a decrease of the central sympathetic activity and the moderate fall in blood pressure. At a higher dosage the absence of increasing hypotensive effect in spite of increasing sympathetic inhibition is probably caused by a stimulation of peripheral postsynaptic alpha-adrenoreceptors.

Animals↗