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  • 1980-1984  (2)
  • Anastomotic dehiscence  (1)
  • Brain stem  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 320 (1982), S. 26-33 
    ISSN: 1432-1912
    Keywords: Convulsions ; Noradrenaline release ; Cerebral cortex ; Brain stem ; MOPEG levels ; Quaking mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The Quaking mouse is a genetically determined model of convulsive disorders. We investigated the modulation of noradrenergic neurotransmission through α2-adrenoceptors in the occipital cortex and the brain stem of this mutant. The endogenous levels of noradrenaline were similar in the cerebral cortex of the Quaking mice and their corresponding controls, while a significant increase of endogenous noradrenaline was found in the brain stem of the mutants. The rate of disappearance of noradrenaline in the cerebral cortex and the brain stem after injection of FLA 63 was identical in control and Quaking mice. The calciumdependent electrically evoked overflow of 3H-noradrenaline from slices of occipital cortex was inhibited by clonidine and enhanced by yohimbine in Quaking as well as in normal mice. The negative feed-back mechanism mediated by presynaptic α2-adrenoceptors operates to a similar extent in both strains of mice. In contrast to the occipital cortex, in the brain stem, the amount of neurotransmitter released by electrical stimulation was significantly increased in Quaking mice when compared with the controls. However, in the brain stem, the negative feed-back regulation of noradrenaline release operates to a similar extent in both strains of mice. When the endogenous levels of MOPEG were determined in the brain stem, they were found to be significantly higher in the Quaking mice when compared to the controls. The results suggest that an increase in noradrenergic neurotransmission in the brain stem, rather than in the cerebral cortex, could contribute to the behavioural abnormalities exhibited by the Quaking mice.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Langenbeck's archives of surgery 358 (1982), S. 253-258 
    ISSN: 1435-2451
    Keywords: Anastomotic dehiscence ; Causes ; Nahtdehiscenz ; Entstehungsmechanismen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der physiologische, biochemische und morphologische Heilungsvorgang der Anastomose ist außerordentlich komplex. Er kann in jeder Phase nachhaltig gestört bis blockiert werden. Nahezu alle Bauelemente sind unter veränderten Konditionen geeignet, eine Insuffizienzentstehung zu begünstigen. Die Insuffizienz kann Folge eines einzelnen gravierenden Störfaktors sein, meist ist sie jedoch das Produkt eines Faktorensynergismus. Gravierende Störfaktoren finden sich im Organsystem Darm selbst, in veränderten biologischen Voraussetzungen und nicht zuletzt in der unzureichenden Taktik und Technik.
    Notes: Summary The healing of intestinal anastomoses has many physiological, biochemical and morphological aspects. In each stage it can be disturbed or blocked. Nearly each factor of normal healing can under changed circumstances, favour anastomotic dehiscence. Dehiscence can be caused by one severe disturbing factor; in most cases, however, there is more than one factor that forms rupture of the anastomosis. The intestine itself can become a disturbing factor as well as changed biological circumstances and last but not least insufficient tactics and techniques of building an anastomosis.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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