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Biomedical subjects

W Wesemann

Publications and source records attributed to W Wesemann.

At least 109 records · Page 6Linked to original sources
PubMed1977

Induction of the platelet release reaction by 1.3-dimethyl-5-aminoadamantane, a new adamantane derivative.

The amantadine derivative 1.3-dimethyl-5-aminoadamantane, D 145, induces in high concentrations of 2-10 mM the release reaction. Adenine nucleotides and 5-hydroxytryptamine (5-HT) are liberated to the same extent and in the same ratio as found after thrombin-induced release. The time course of release is very slow; maximal release is reached in 15-20 min. The process is temperature-dependent and dependent on energy derived from glycolysis and oxidative phosphorylation. Extracellular Ca++ does not promote the release process. D 145, in accordance with the mother-substance amantadine, inhibits 5-HT uptake non-competitively, KI = 0.15mM. In concentrations of 0.1-1 mM D 145 triggers only the liberation of 5-HT, adenine nucleotides are not liberated. The ADP induced platelet aggregation is completely inhibited after preincubation with a 1 mM solution of D 145.

Adamantane↗
PubMed1977

[The action of 1-aminoadamantane. Comparative studies with isolated nerve endings and thrombocytes on the release of serotonin and dopamine].

Nerve endings isolated from rat brain accumulate exogenous serotonin and dopamine. Both biogenic amines are released from nerve endings as well by means of electrical stimulation with rectangular pulses of alternating polarity as by incubation with 5 X 10(-4) to 5 X 10(-5) M solutions of the adamantane derivatives 1-aminoadamantane hydrochloride (D 1) and 1-amino-3,5-dimethyladamantane hydrochloride (memantine, D 145). The electrically stimulated liberation is small but is significantly increased after simultaneous incubation of the nerve endings with subthreshold concentrations of 1-aminoadamantanes (5X10(-6) to 5X10(-5) M). The reuptake of released serotonin is noncompetitively inhibited by 1-aminoadamantanes. Also in blood platelets frequently used as model cells of the nerve endings the serotonin uptake is inhibited by small concentrations of D 145, 10(-5) to 2X10(-4) M. High concentrations of D 145- greater than 2X10(-3) M, induce the "release-reaction", the simultaneous liberation of serotonin, ATP, and ADP. In the concentration range of 2X10(-4) to 2X10(-3) M D 145 only serotonin is set free.

Amantadine↗
PubMed1975

Studies on serotonin binding proteins of nerve ending membranes.

Synaptic membranes were isolated from rat brain homogenates by differential and density gradient centrifugation. Membrane proteins were solubilized by detergent buffer and assayed for serotonin-binding activity by adsorption of free 5-HT on charcoal. When the membrane extract was incubated with serotonin at +4 degrees C for various times, equilibrium was reached within 10 min. With increasing serotonin concentrations the specific part of binding was saturable whereas the non-specific part increased linear with the total 5-HT added. Kinetic analysis of the data revealed two different classes of binding sites with the apparent dissociation constants Kd1 = 5.3X10(-7) M and Kd2 = 1.1X10-5 M. The disociation reaction followed first order kinetics in two steps. The first step was very rapid, the second step proceeded with a half life time t1/2 of 16 min and a dissociation rate constant of k-1 = 7.2X10(-4) s-1. the binding was sensitive to heat and SH-blocking reagents and displaceable by serotonin in excess, d-LSD, and to a lower extent by 5-methoxytryptamine and tryptamine. The significance and localization of the binding sites at the membrane are discussed.

Animals↗
PubMed1975

Serotonin uptake and release by biochemically characterized nerve endings isolated from rat brain by concomitant flotation and sedimentation centrifugation.

Crude synaptosomal preparations of rat brain were separated by concomitant flotation and sedimentation in a sucrose gradient into fractions containing myelin, nerve endings, and mitochondria, respectively. Two myelin-free nerve ending fractions were obtained which differ in the serotonin content and the activities of the enzymes 5-hydroxytryptophan decarboxylase, monoamine oxidase, choline acetylase, and acetylcholin-esterase. In glucose medium sodium ions stimulate serotonin uptake into the nerve endings while potassium ions in sucrose solution induce the release of this amine.

Acetylcholinesterase↗
PubMed1975

[Permanent registration of the energy transformation in patients with skull-brain injuries and brain tumors].

By means of a measuring device based on the principles of indirect calorimetry, long-term recording of energy transformation in patients with cerebral tumours and cerebral traumas is performed. Contrary to the conception that the catabolic state in the postoperative/posttraumatic period corresponds to a negative balance between requirement and enteral/parenteral supply, it appears that, as a rule, the energy requirement is only 1 to 1 1/2 times higher than under normal conditions. During long-term measurement, clinical phenomena that are characterized by increased muscular activity (seizures, extension automatisms, extreme psychomotor excitations) show a daily requirement of maximal 3,500 kcal. Considering the clearly lower requirement, the change of the catabolic state by a high-caloric intake (5,000 and 6,000 calories/day) can only be due to an effect on the regulation of the metabolic processes.

Basal Metabolism↗