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Biomedical subjects

A Lehmann

Publications and source records attributed to A Lehmann.

At least 145 records · Page 8Linked to original sources
PubMed1985

N-Methylaspartate-evoked liberation of taurine and phosphoethanolamine in vivo: site of release.

The effect of N-methyl-D,L-aspartic acid (NMA) on extracellular amino acids was studied in the rabbit hippocampus with the brain dialysis technique. Administration of 0.5 or 5 mM NMA caused a concentration-dependent liberation of taurine and phosphoethanolamine (PEA). Taurine increased by 1,200% and PEA by 2,400% during perfusion with 5 mM NMA whereas most other amino acids rose by 20-100%. The effect of NMA appeared to be receptor-mediated, as coperfusion with D-2-amino-5-phosphonovaleric acid curtailed the NMA response by some 90%. The NMA-stimulated release of taurine and PEA was suppressed when Ca2+ was omitted and further inhibited when Co2+ was included in the perfusion medium. The effect of NMA was mimicked by the endogenous NMA agonist quinolinic acid and the partial NMA agonist D,L-cis-2,3-piperidine dicarboxylic acid. Although the NMA-evoked release of taurine and PEA was Ca2+-dependent in vivo, NMA had no effect on Ca2+ accumulation in hippocampal synaptosomes. The previously reported NMA-induced activation of dendritic Ca2+ spikes and the lack of effect on synaptosomal Ca2+ uptake suggest that taurine and PEA are released from sites other than nerve terminals, possibly from dendrosomatic sites. This notion was strengthened by the absence of an effect of NMA on the efflux of radiolabelled taurine from hippocampal synaptosomes. In contrast, high K+ stimulated synaptosomal uptake of Ca2+ and release of taurine.

Animals↗
PubMed1984

A role for taurine in the maintenance of homeostasis in the central nervous system during hyperexcitation?

Employing the brain dialysis technique, we demonstrate that the aspartate congener N-methyl-D,L-aspartic acid (NMA) stimulates the release of endogenous taurine in vivo in a Ca2+-dependent manner. Furthermore, exogenous taurine (1-10 mM) inhibits the NMA-induced Ca2+ influx into intracellular compartments. This suggests that the extracellular taurine concentration may control Ca2+ movement and thereby provide a homeostatic mechanism in situations of excessive excitation.

Animals↗
PubMed1984

Inhibition by verapamil of ischemic Ca2+ uptake in the rabbit hippocampus.

In the study described here a perfusion-dialysis system was used for recording ionic changes in the hippocampus during ischemia. Local perfusion with a Ca2+ entry blocker (verapamil) inhibited the fall in extracellular Ca2+ concentration which occurs in ischemia. The data consequently suggest that intracellular Ca2+ accumulation during ischemia can be blocked. A Ca2+ antagonist such as verapamil may thus improve post-ischemic neuronal recovery via a direct effect on parenchymal cells in addition to the previously suggested vascular effects.

Animals↗
PubMed1984

A possible interrelationship between extracellular taurine and phosphoethanolamine in the hippocampus.

The effect of guanidinoethane sulfonic acid (GES), an inhibitor of taurine uptake, was examined with respect to endogenous amino acids in the hippocampus of the freely moving rabbit. GES increased the extracellular levels of both taurine and phosphoethanolamine (PEA), other amino acids being unaffected. However, long-term oral administration of GES selectively reduced endogenous taurine levels. The effect of GES on PEA appeared to be a consequence of the elevated extracellular taurine as exogenously administered taurine per se increased PEA levels in the extracellular space. The findings are discussed in conjunction with the proposed membrane-stabilizing effects of taurine.

Animals↗
PubMed1984

Inhibition of cholinergic response by taurine in frog isolated skeletal muscle.

Carbamylcholine-stimulated contractions of isolated frog gastrocnemius muscle were inhibited in a non-competitive fashion by 5-25 mM taurine. Taurine had no effect on the resting length of the muscle. Caffeine-induced contractures were unaffected by taurine which indicates that the sarcoplasmic reticulum is not an important site of action for taurine. A possible functional role for taurine in skeletal muscle is discussed.

Animals↗
PubMed1984

Capillary blood flow in the amelanotic melanoma of the hamster after isovolemic hemodilution.

In malignant tumors, spontaneous arteriolar vasomotion disappeared already during earliest tumor growth (tumor weight less than 200 mg) suggesting that arterioles supplying a malignant tumor with blood are maximally dilated from the very beginning of tumor growth. As a result, the viscosity of blood becomes a limiting factor of tissue perfusion. To evaluate the effects of isovolemic hemodilution in a malignant tumor, a transparent chamber model was used in conjunction with a subcutaneously growing amelanotic melanoma of the hamster. Quantitative intravital microscopy (video image analysis) and a platinum multiwire electrode were utilized to study the tumor microcirculation. Isovolemic hemodilution was performed by exchange of blood vs. Dextran 60 to lower the systemic hematocrit to 30% in 21 animals. Capillary flow increased significantly and improved tissue pO2 on the tumor's surface without any change in capillary density. Since tumor growth was accelerated after hemodilution, these data suggest to combine with hemodilution other treatment modalities to improve blood-mediated tumor therapy.

Animals↗
PubMed1983

Dihydrokainic acid affects extracellular taurine and phosphoethanolamine levels in the hippocampus.

The specificity of the inhibitory effect of dihydrokainic acid on the high-affinity glutamate uptake was tested in an in vivo system. The rabbit hippocampus was perfused with Krebs--Ringer bicarbonate medium to which dihydrokainic acid was added (final concentrations 1 and 5 mM) with or without depolarizing potassium concentrations. Dihydrokainate elevated the levels of glutamate, taurine and phosphoethanolamine. This response was partly similar to that observed after high potassium administration. The selectivity of dihydrokainic acid is thus not restricted to glutamate, and its value as a tool in the study of glutamatergic transmission is discussed.

Animals↗
PubMed1983

Effects of in vivo administration of kainic acid on the extracellular amino acid pool in the rabbit hippocampus.

The effect of local administration of kainic acid in the rabbit hippocampus was studied; the hippocampus was perfused continuously in the freely moving animal with an implanted 0.3-mm dialysis fiber. The pattern of endogenous amino acids in the perfusate, reflecting extracellular amino acids, was monitored with liquid chromatography separation and fluorimetric detection of amino acid derivatives. Kainic acid was included in the perfusion medium for up to 70 min at 0.1-1.0 mM and, with time, induced epileptiform activity. Endogenous glutamic acid, taurine, and phosphoethanolamine levels were increased selectively at the lower perfusion concentrations of kainic acid. Long perfusion periods with higher concentrations increased the levels of virtually all amino acids. Perfusion of the hippocampus with depolarizing concentrations of potassium gave an amino acid response partly similar to that seen with kainic acid treatment. However, one notable difference between the two responses was that the extracellular concentration of glutamine, although not influenced by kainic acid, was significantly decreased after high potassium concentrations. These results confirm previous notions that kainic acid has a primarily excitatory effect, one manifestation of this effect being the release of glutamic acid.

Amino Acids↗