Biomedical subjects
Publications and source records attributed to H Breuer.
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[4-14C] Oestradiol-17 beta was perfused through isolated brains of male and ovariectomized female rats. Two different perfusion media were used. The uptake of oestradiol-17 beta was higher in female brains, the highest concentrations being found in the hypophysis and hypothalamus. Oestradiol-17 beta was metabolized to a greater extent by female brains, the most important metabolite being oestrone. Additionally, 2-hydroxyoestradiol-17 beta, 6 zeta-hydroxyoestradiol-17 beta, and 7 alpha-hydroxyoestradiol-17 beta were found; 7 alpha-hydroxyoestrone and another polar metabolite could not be definitely identified. Quantitatively, 2-hydroxylation was no more important than hydroxylation at C atom 6 or 7.
Rats were treated with reserpine, desmethyl-imipramine, or carrier, either alone or in combination with tropolone. Either 10 min (t1) or 1 h (t2) after intraventricular injection of [3H]noradrenaline, they were decapitated. The total 3H activity and the recovery of [3H]noradrenaline were determined in tissue extracts from various brain regions. Maximum total 3H activity was measured at t1 in all tropolone-treated rats; the mean sum of these results served as an estimate of the initial tissue concentration of [3H]noradrenaline. At t1, 40-50% of the sum of [3H]noradrenaline and its metabolites was recovered unchanged in normal rats; reserpine and DMI reduced the recovery to 18-27%. In all groups, the decline of [3H]noradrenaline was retarded after t1. Inhibition of catechol-O-methyltransferase by tropolone caused consistently elevated [3H]noradrenaline levels, but did not affect the metabolic rate after t1 when compared with similarly pretreated, but tropolone-free rats. Thus, if catechol-O-methyltransferase was inhibited during the injection of [3H]noradrenaline, a higher percentage of the amine had been taken up into spaces with a slow noradrenaline turnover. The maximum increase was seen when the neuronal uptake1 was inhibited by desmethylimipramine. This supported the hypothesis that an additional extraneuronal space exists, in addition to the known intraneuronal and extraneuronal compartments, which has a slow noradrenaline turnover. The tropolone effect on the noradrenaline recovery possibly shows that there might be a saturable "methylating system," similar to that described for the periphery, in which catechol-O-methyltransferase is linked to the extraneuronal uptake2.(ABSTRACT TRUNCATED AT 250 WORDS)
Rats were pretreated with either reserpine or desmethylimipramine, either alone or in combination with tropolone. At either 10 min or 1 h after the intraventricular injection of [3H]noradrenaline, in several brain regions the complete metabolic patterns were determined: normetanephrine; the glycol metabolites (methylated and nonmethylated) and their sulfate conjugates; and the acidic metabolites (methylated and non-methylated). A reserpine-induced increase in the turnover of [3H]noradrenaline caused a transient increase of the catechol glycol followed by elevated levels of the two glycol sulfates. The stimulated [3H]noradrenaline turnover if achieved by desmethylimipramine caused a transient increase of normetanephrine and initially lowered values of catechol glycols (both free and sulfated), which were followed by elevated levels. Drug-pretreated rats compensated for the inhibition of catechol-O-methyl-transferase by tropolone in different ways: Reserpine caused an early increase of the catechol glycol beyond the measurements in other treatment groups, whereas desmethylimipramine increased the nonmethylated carboxylic acid and glycol sulfates rather slowly to levels beyond those of other groups. The results support the existence of two compartments with a fast metabolism (an intraneuronal monoamine oxidase compartment and an extraneuronal catechol-O-methyltransferase compartment). In addition, there seems to exist another extra-neuronal space with a slow, monoamine oxidase-dependent noradrenaline turnover.
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Carcinoembryonic antigen (CEA) was localized in various embryonic and fetal human tissues between 8 and 16 weeks of gestation as well as in the colorectal mucosa of older fetuses, newborns and adults. Among the embryonic tissues, CEA was always present in the esophagus, the gastric antrum, the duodenum and the rectum. CEA positive staining of bile canaliculi of the liver was inconstant. All other embryonic tissues were CEA negative. During early fetal development, CEA positive staining of the esophagus, antrum and duodenum was inconstant. However, the whole colon became intensively stained. An inconstant CEA specific staining was found in parts of the midgut and in the bile canaliculi of the liver. The other organs remained CEA negative. Between the 17th week of gestation and birth, CEA staining pattern of the colorectal mucosa did not change. The staining intensity of late fetal colonic mucosa was similar to that of adult colonic mucosa.
A method for the perfusion of the isolated brain of the rat with synthetic fluorocarbon emulsion is described. The functional states of the brains were investigated using biochemical, biophysical, and histological methods. After 4.5 h of perfusion, all brains were in excellent condition and comparable to the in vivo state. The influence of perfusion conditions on the viability of the brains was studied. Deep hypothermia was well tolerated; at 13 degrees the EEG exhibited a mean frequency of about 8 Hz, while the mean amplitude was about 40% lower than at 28 degrees or 36 degrees. Constant-pressure perfusion did not affect brain function, provided that the pressure amplitude was very slowly decreased. During application of pentylenetetrazole (PTZ) it was found that the threshold concentration of PTZ in the perfusion medium to induce epileptic seizure discharges was 0.13 mg/ml. However, after repeated application of PTZ, the threshold concentration decreased exponentially, indicating a kindling phenomenon. It could be shown that not PTZ as such, but the spike potentials provoked by PTZ, induced the kindling effect. This was inhibited by application of primidone or phenobarbital.
In the years 1977 to 1981, 14 quality-control surveys for the determination of steroid hormones were performed in cooperation with the Deutsche Gesellschaft für Klinische Chemie. Hereby the laboratories participating could in each case analyze the following steroids: aldosterone, cortisol, oestradiol-17 beta, oestriol, progesterone, and testosterone. In the light of the results an investigation was made as to whether, in the course of time, an improvement in the accuracy or in the precision of the determinations had been attained, and to what extent the determinations depend on the qualities of the test material. A clear improvement in the accuracy of the results of the analyses could only be ascertained for oestradiol-17 beta. For aldosterone and cortisol, values were found in pool-plasma whose medians were significantly above the definitive values. An improvement in precision could be noted especially with oestradiol-17 beta and to lesser degrees with cortisol and oestriol. The kind of test material--plasma which contained only the hormones to be analyzed on the one hand, and, on the other hand, pool-plasma, which also contained all endogenous hormones--had no influence on the precision of the results from various laboratories. Low concentrations of the individual steroids led--on the basis of the methodological principle of radioimmunoassays--in almost all cases to a reduced interlaboratory precision in regard to values. The accuracy of the analysis values was considerably impaired only with aldosterone and oestradiol-17 beta by low concentrations: the medians here were in part twice as high as the definitive values.
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A Central American cattle paralysis is produced by ingestion of the plant Melochia pyramidata L. (Sterculiaceae). Its main alkaloid "melochinine" has been shown to produce paralysis, bradypnea, bradycardia and hypotension in laboratory animals after p.o., i.p. and i.v. applications. Bradycardia and negative inotropia have been demonstrated in isolated guinea pig atria and paralysis in the isolated phrenic nerve diaphragma preparation as well as in the phrenic nerve in situ preparation with local application. Gas chromatographic measurements suggest a rapid disappearance of melochinine after intravenous application and showed the similarity of the biologically active melochinine concentrations in vivo and in vitro. No unchanged melochinine was found in the urines of mice by thin-layer chromatography. A slight inhibition of the mitochondrial respiration and of some cholinesterases and none of the ATPase was found. Melochinine does not reveal insecticidal activity as does its structural analogue piericidin A, a well known inhibitor of the mitochondrial respiratory chain. The action of the alkaloid may be explained by an unspecific interaction with membranes, partially responsible for a Ca2+-antagonistic effect found in the isolated guinea pig papillary muscle. The proposed non-specific action could be a possible reason for the fact that trials of a specific therapy failed in our experiments.
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The binding of [125I]CEA to an anti-CEA Sepharose-4B immunosorbent has been investigated in the presence of detergents. Non-ionic detergents (Triton-X-100, Lubrol PX and Tørgitol NPX) at concentrations of 5-40 milligrams did not inhibit the binding of [125I]CEA to the immunosorbent. Sodium deoxycholate decreased the binding from 98% (concentration of detergent 0.6 milligram) to 41% (concentration of detergent 20 milligrams). Sodium dodecyl sulfate inhibited the binding of [125I]CEA to the immunosorbent considerably, even at low concentrations.
A definitive method is described for the determination of cortisol in human plasma. The method is based on the principle of isotope dilution-mass spectrometry. The analytical procedure comprises the following steps: (1) Addition of [4-14C]cortisol to the plasma sample; (2) extraction of the 14C-labelled and of the non-labelled cortisol by dichloromethane; (3) purification of the cortisol fraction by column chromatography on Sephadex LH-20; (4) formation of the trimethylsilyl ether of cortisol methoxime; (5) selected ion monitoring at m/z-values 605, 607, 636 and 638 during gas liquid chromatography. The accuracy of the method is based on the high specificity of mass spectrometry and on the exact control of recovery employing the principle of isotope dilution. The precision of the method was evaluated by calculation of the coefficient of variation from day to day; this varied from 0.7-2.3% in the range of 256-845 nmol/l. The lower limit of detection (ratio of signal to noise 3:1) is 200 pg cortisol per sample.
The effects of oestradiol-17 beta, 2-hydroxyoestradiol-17 beta and 2-methoxyoestradiol-17 beta on the metabolism of [3H]noradrenaline were studied in various brain regions of ovariectomized in rats in vivo. Under the experimental conditions chosen, oestradiol-17 beta had no effect on the metabolic pattern of noradrenaline. After pre-treatment of ovariectomized rats with 2-hydroxyoestradiol-17 beta, the formation of methylate metabolites of noradrenaline (normetanephrine and 3-methoxy-4-hydroxyphenylglycol sulphate) was reduced, whereas that of non-methylated products (3,4-dihydroxymandelic acid and 3,4-dihydroxyphenylglycol sulphate) was increased. The inhibition of methylation was most pronounced in posterior hypothalamus and less significant in anterior hypothalamus and thalamus. Pre-treatment with 2-methoxyoestradiol-17 beta yielded inconsistent results. From the findings described here it may be concluded that 2-hydroxyoestradiol-17 beta, as previously shown in vitro, also affects the metabolism of noradrenaline in vivo by directly interacting with the catechol-O-methyltransferase. It is suggested that this metabolic effect may be responsible - at least to some extent - for the inhibitory effect of 2-hydroxyoestradiol-17 beta on LH secretion.