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  • 1985-1989  (2)
  • 1986  (2)
  • Eicosanoids  (1)
  • Regeneration  (1)
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Years
  • 1985-1989  (2)
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 12 (1986), S. 116-126 
    ISSN: 1432-1238
    Keywords: Eicosanoids ; Survival ; Clinical ; Animal
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intravenous bolus endotoxin elicits a marked but transient increase in plasma TxB2 and 6-keto-PGF1α in a large number of species. A smaller, delayed and more prolonged increase in TxB2 and 6-keto-PGF1α are reported in animals with septic shock, i.e., those with fecal peritonitis or cecal ligation. Thromboxane synthetase inhibitors or antagonists attenuate endotoxin-induced acute cardiopulmonary changes, the delayed increase in serum lysosomal enzymes, fibrin/fibrinogen degradation products and the thrombocytopenia in a number of species. While these drugs increase survival of rats or mice following endotoxin they do not alter survival of rats in septic shock. These results support the hypothesis that TxA2 exerts a pathophysiologic effect in shock following bolus endotoxin. In contrast, nonsteroidal antiinflammatory drugs (NSAID) and dietary essential fatty acid deficiency increase survival of rats subjected to endotoxin shock, and survival time in models of septic shock. These results also suggest that some other cyclooxygenase product(s) is involved in septic shock due to fecal peritonitis or cecal ligation. Preliminary experimental studies indicate salutary effects of leukotriene inhibitors and antagonists in endotoxin shock and in models of acute pulmonary injury. Clinical studies have demonstrated elevated plasma TxB2 and 6-keo-PGF1α concentrations in patients with septic shock, and elevated LTD4 in pulmonary edema fluid of patients with the adult respiratory distress syndrome. In view of these clinical and experimental results, clinical trials of NSAID and/or leukotriene inhibitors/antagonists should be considered.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Retinotectal projection ; Regeneration ; Topography ; Goldfish
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The topographic precision of the regenerating retinotectal projection of the goldfish was studied between 18 and 524 days (at 20° C) after optic nerve cut, using retrograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase (WGA-HRP) from one of two standardized tectal injection sites. All labelled ganglion cells in each flat-mounted retina were plotted individually, and their degree of dispersion was assessed by a statistical method based on distance to nearest neighbour. Labelled cells in normal fish were clustered tightly, covering on average only 1.3% of the retina. Early in regeneration (18–28 days) they were widely dispersed, covering up to 75.2%, and they did not begin to form recognizable clusters at appropriate sites until about 35 days after nerve cut. Between 18 and 70 days, the proportion of retina covered by labelled cells fell dramatically, halving about every 14 days. Between 70 and 524 days, no further reduction could be demonstrated: overall, clusters remained significantly larger than normal, though a few individual retinae were virtually normal. Several others, labelled from similar single injections between 56 and 524 days after nerve cut, showed pairs of cell clusters; a sign that persistent errors in topography are common. The very wide initial scatter of labelled cells reflects a striking lack of ‘goal-directedness’ in regenerative axon growth. Extensive branching in the optic nerve, tract and tectum, for which there is already evidence, must contribute to this. Though uptake of some WGA-HRP by non-synaptic growth cones cannot be ruled out, other evidence for mislocated functional synapses at early stages encourages us to favour ‘trial and error’ synapse formation as the likely basis of map refinement.
    Type of Medium: Electronic Resource
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