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  • 1
    ISSN: 1432-1246
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Untersuchungen an freiwilligen Versuchspersonen unter überdruck sollten zur Klärung der Frage beitragen, ob Kohlenoxid bei Einatmung gleicher CO-Luftgemische unter erhöhtem Druck giftiger ist als unter normalem atmosphärischem Druck (1 ata). Die Versuche mit CO-Konzentrationen von 50 sowie 100 ppm bei 1 ata und 3 ata wurden in einer 8,3 m3 großen Druckkammer vorgenommen, in der die O2-, CO2- und CO-Konzentrationen während der Exposition überwacht wurden. Bei Messung der CO-Konzentration in der Alveolarluft und des COHb-Wertes im Blut zeigt sich, daß die Sättigung des Blutes mit CO — wie auch die Einstellung des Diffusionsgleichgewichtes im Organismus — bei 3 ata erheblich schneller erfolgt als unter dem Druck von 1 ata. Bei Einatmung von 100 ppm CO beträgt beispielsweise die CO-Konzentration in der Alveolarluft der unter 3 ata atmenden Probanden nach 2 Std 73 ppm, bei den unter 1 ata atmenden Probanden jedoch nur 36,7 ppm CO. Dieses Ergebnis erklärt sich aus dem erhöhten CO-Angebot bei erhöhtem CO-Partialdruck. Hervorzuheben ist der Befund, daß die COHb-Konzentration im Diffusionsgleichgewicht unter erhöhtem Druck signifikant niedriger liegt als unter normalem Druck (p〈0,001). Im Diffusionsgleichgewicht findet man beispielsweise bei Einatmung von 50 ppm CO bei 3 ata einen COHb-Wert von 4,5%, bei 1 ata dagegen von 7,25 %. Dieses Ergebnis läßt sich mit der Konkurrenzreaktion von CO und O2 um den Receptor Hämoglobin erklären, die dem Massenwirkungsgesetz unterliegt. Es besteht somit nach unseren Ergebnissen kein Grund, den MAK-Wert von 50 ppm CO bei Arbeiten unter erhöhtem atmosphärischem Druck zu senken.
    Notes: Summary On healthy volunteers we investigated whether carbon monoxide would be more toxic under increased pressure than under normal pressure, if this gas is inspired at the same concentration under both conditions. It was shown by measurements of CO concentration in alveolar air and of the CO-Hb content of blood that under 3 ata the blood is saturated faster with carbon monoxide than under normal atmospheric pressure, indicating that under increased pressure diffusion equilibrium in the organism is achivied earlier. In subjects breathing 100 ppm CO for 2 hours the CO concentration in alveolar air is 73 ppm under 3 ata and not more than 36.7 ppm at 1 ata. This result is explained by the increased CO supply under increased pressure. It must be emphasized that the CO-Hb concentration is significantly lower under increased pressure than under atmospheric pressure (p〈0.001), once diffusion equilibrium has been attained. In subjects breathing 50 ppm CO the CO-Hb concentration is only 4.5 % at 3 ata but 7.25 % at 1 ata. This result is explained by application of the law of mass action on the competition of CO and O2 for the receptor hemoglobin in the blood. It must be concluded from our experimental data that there is no reason to lower the threshold limit value of 50 ppm CO for work carried out under increased pressure.
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  • 2
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mouse brain cortex slices preincubated with3H-noradrenaline were superfused and the effect of histamine on the electrically (0.3 or 3 Hz) evoked tritium overflow was examined. The evoked overflow was inhibited by histamine and R-(−)-α-methylhistamine but not by 2-(2-thiazolyl)ethylamine and dimaprit. The effect of histamine was antagonized by thioperamide but not by dimethindene and ranitidine. The degree of inhibition produced by histamine was more marked at 0.3 than at 3 Hz and was attenuated by the α2-adrenoceptor agonist talipexole (the former B-HT 920) but increased by phentolamine and the α2-adrenoceptor antagonist rauwolscine. Pre-exposure of slices toN-ethylmaleimide attenuated the inhibitory effect of histamine. The results suggest that histamine inhibits nordrenaline release in the mouse brain cortex via H3 receptors which interact with presynaptic α2-adrenoceptor and may be coupled to a G (e.g. Gi or Go) protein. The extent of H3 receptor-mediated inhibition of nordrenaline release in the mouse brain is more marked than that in the rat brain.
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  • 3
    ISSN: 1432-0738
    Keywords: Carbon Monoxide in Blood and Alveolar Air ; Law of Mass Action ; Psychological Effects ; Kohlenoxid in Blut und Alveolarluft ; Massenwirkungsgesetz ; Psychologische Auswirkungen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An freiwilligen Versuchspersonen, die keine körperliche Arbeit leisten, wird die Aufnahme von Kohlenoxid während und nach Einwirkung von 100 ppm CO in Luft untersucht. Gleichzeitig werden die psychologischen Auswirkungen unter dieser CO-Konzentration geprüft. Nach 8 Std ist das Diffusionsgleichgewicht im Organismus noch nicht erreicht. Die höchste von uns gemessene COHb-Konzentration beträgt zu diesem Zeitpunkt 11,6%. Annähernd lineare Beziehungen zwischen dem COHb-Gehalt und der CO-Konzentration in der Ausatmungs- bzw. Alveolarluft bestehen nur für begrenzte Konzentrationsbereiche. Rückschlüsse von der CO-Konzentration in der Exspirationsluft auf den COHb-Gehalt des Blutes auf der Grundlage einer linearen Korrelation über größere Konzentrationsbereiche können wegen der in Wirklichkeit exponentiellen Abhängigkeit zwischen beiden Größen mit hohem Schätzfehler belastet sein. Anhand einer Stichprobe von 42 Studenten hat sich zeigen lassen, daß Kohlenoxid in einer Konzentration von 100 ppm nach einer Expositionsdauer von 21/2 Std zu Leistungsminderungen in der visuellen Wahrnehmung, der Handfingergeschicklichkeit, der Lernfähigkeit und bestimmten Intelligenzleistungen führt. Zu diesem Zeitpunkt wird eine alveolare CO-Konzentration von 55 ppm und ein COHb-Wert von 7,2% gemessen. Subjektive Symptome fehlen im allgemeinen; Raucher und Nichtraucher unterscheiden sich hinsichtlich ihrer psychologischen Beeinflußbarkeit durch 100 ppm CO nicht. Die beobachteten Effekte lassen sich nach unseren derzeitigen Kenntnissen nicht zwanglos als reine Hypoxiewirkung erklären. Es wird diskutiert, ob die Beeinflussung enzymatischer Stoffwechselreaktionen im Gewebe ursächlich eine Rolle spielt.
    Notes: Abstract In experiments on healthy volunteers 19 to 34 years of age seated quietly in a closed chamber of 1.5 m3 capacity continuously circulated with a mixture of air and CO, the uptake and psychological effects of carbon monoxide during and after exposure were investigated. After 8 hours of breathing 100 ppm CO, a concentration of 93 ppm was measured in expiratory alveolar air, demonstrating that diffusion equilibrium in the organism had not yet been attained. The highest concentration of CO-Hb measured under these experimental conditions was 11.6%. It was calculated by applying the law of mass action that only within a limited range of CO concentrations is there an approximate linear relation between the CO concentration in expired air and the CO-Hb content of blood. Any conclusions as to the CO-Hb content of blood drawn from the known CO concentration of expired air assuming a linear correlation between the two over a greater range of concentrations are bound to be burdened with considerable error, since in reality the relationship between the two quantities is an exponential one. On the basis of tests carried out on a random sample of 42 students, it could be shown that carbon monoxide inspired in concentration of 100 ppm for 21/2 hours resulted in a statistically significant diminution of visual perception, manual dexterity, ability to learn and perform certain intellectual tasks. At this time, the measured CO concentration in alveolar air was 55 ppm and the CO-Hb level was 7.2%. Subjective symptoms were generally absent. Smokers and non-smokers showed no discernable differances in regards to their psychological susceptibility by 100 ppm CO. The observed effects cannot be satisfactorly explained, at least in our present state of knowledge, on the basis of hypoxia alone.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 24 (1969), S. 260-270 
    ISSN: 1432-0738
    Keywords: Carbon Monoxide Affinity to Hemoglobin ; Carbon Monoxide in Tissue ; Carbon Monoxide in Expired Air ; Law of Mass Action ; Kohlenoxidaffinität des Hämoglobins ; Kohlenoxid im Gewebe ; Kohlenoxid in der Ausatmungsluft ; Massenwirkungsgesetz
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In Versuchen an Kaninchen wird die Aufnahme, Verteilung und Abgabe von Kohlenoxid untersucht und zwar durch Analysen von Proben der Ausatmungsluft, des Blutes und eines künstlich angelegten intraperitonealen Stickstoffdepots. Im Pneumoperitoneum stellt sich während der Beatmung mit konstanten CO-Luftgemischen der Gleichgewichtspartialdruck für CO erst nach etwa 15 Std ein, und auch die Ausscheidung aus dem Depot dauert länger als 10 Std. Der Gleichgewichtspartialdruck für CO im Gewebe beträgt bei Beatmung mit 0,212 Torr CO (CO-Konzentration = 300 ppm) nur 64% des CO-Partialdrucks in der Einatmungsluft, bei Beatmung mit 0,708 Torr CO (CO-Konzentration = 1000 ppm) sogar nur 47% des CO-Partialdrucks in der Einatmungsluft. Nach Einstellung des Diffusionsgleichgewichts liegt der CO-Partialdruck im Gewebe bei den einzelnen Tieren um so höher, je geringer die Affinität des Hämoglobins zum Kohlenoxid ist. Diese Beziehung gilt auch für verschiedene Tierspezies. Experimentell und an Hand des Massenwirkungsgesetzes wird bewiesen, daß die Konkurrenz des Kohlenoxids und des Sauerstoffs um den Receptor Hämoglobin auch für den CO-Partialdruck im Gewebe ein wesentlicher determinierender Faktor ist.
    Notes: Summary The uptake, distribution and elimination of carbon monoxide (CO) was investigated in experiments with rabbits by analysing samples of expired air, blood and a pneumoperitoneum of nitrogen set the day before. The partial pressure of CO in a pneumoperitoneum first reaches equilibrium after approx. 15 hours of breathing a constant mixture of CO and air. The excretion of CO from this area also requires more than 10 hours. The partial pressure of CO in the tissues reaches 64% of that of the air inspired at a CO pressure of 0.212 Torr (CO concentration of 300 ppm); it attains only 47% of the CO partial pressure of the inspired air if the animals breathe a. mixture with 0.708 Torr CO (CO concentration of 1,000 ppm). The less affinity the hemoglobin of individual animals has for carbon monoxide, the higher the CO partial pressure in the tissues, once diffusion equilibrium has been achieved. This correlation holds also true for different animal species. It has been proven by experimentation and by application of the law of mass action that the competition between carbon monoxide and oxygen for the receptor hemoglobin also represents an essential factor in the determination of CO partial pressure in the tissues.
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  • 5
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Pentobarbital concentrations of 10–100 μM selectively inhibited the noradrenaline release evoked by activation of the nicotinic receptors on the terminals sympathetic nerves of the rabbit heart. Higher concentrations also decreased the noradrenaline release induced by KCl or by electrical stimulation of the nerve axons.
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  • 6
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Morphine inhibited the noradrenaline release from slices of rat brain cortex induced by introduction of Ca2+ ions after superfusion with Ca2+-free, K+-rich solution. The degree of inhibition was inversely related to the Ca2+ concentration used for stimulation.
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  • 7
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
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  • 8
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
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  • 9
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 288 (1980), S. 86-88 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Slices of hypothalamus or occipital cortex (0.3 mm thick, diameters 2.0 and 3.0 mm, respectively) from male Wistar rats (200-300 g) were incubated for 60 min in physiological salt solution (of composition described in Fig. 1 legend) containing one of the following tritiated monoamines ai a ...
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  • 10
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Slices from human neocortex preincubated with [3H]serotonin ([3H]5-HT) were superfused and stimulated electrically to investigate whether the α2-adrenoceptors on serotonergic terminals can be stimulated by endogenous noradrenaline (NA) released from neighboring noradrenergic fibers. The stimulation-evoked 3H overflow, representing action potential-induced, exocytotic release of 5-HT, was depressed by the NA uptake blocker (+)-oxaprotiline. Rauwolscine (a mixed α2-adrenoceptor antagonist/5-HT autoreceptor agonist) or phentolamine [a combined α- adrenoceptor/5-HT autoreceptor antagonist; the latter drug in the presence of (+)-oxaprotiline] enhanced the release when the 5-HT autoreceptors had previously been blocked by metitepine. Under hypothermia the release of 5-HT was found to be decreased and that of NA to be increased; under these conditions idazoxan (an α2-adrenoceptor antagonist) enhanced the release of 5-HT. In neocortex slices from rats (+)-oxaprotiline similarly depressed the release of 5-HT (measured with the same methods) as in human tissue. When rats were pretreated with 6-hydroxydopamine, the inhibitory effect of exogenous NA on 5-HT release was increased, and in slices from rats pretreated with desipramine, it was decreased. In conclusion, α2-heteroreceptors can be activated by endogenous NA released from neighboring noradrenergic fibers. Because regulatory processes analogous to those in rats probably occur in humans as well, an up- or down-regulation of α2- heteroreceptors in depressed patients with a (pathological) decrease or a (therapeutic) enhancement of the noradrenergic neurotransmission may also be assumed to occur.
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