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  • Articles: DFG German National Licenses  (3)
  • 1995-1999  (3)
  • L-NAME  (2)
  • Bioavailable  (1)
Source
  • Articles: DFG German National Licenses  (3)
Material
Years
  • 1995-1999  (3)
Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Heavy metal history from cores in Wellington Harbour, New Zealand (1996)
    Springer
    Environmental geology 27 (1996), S. 59-69 
    Details
    ISSN: 1432-0495
    Keywords: Heavy metal ; Core ; Wellington, New Zealand ; Bioavailable ; X-ray fluorescence ; Acid leaching ; Estuary ; Index of geoaccumulation ; I geo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences
    Notes: Abstract Analysis of ten heavy metals (Ag, Cd, Cr, Cu, Fe, Mn, Ni, Pb, Sb, Zn) in six sediment cores from Wellington Harbour show both anthropogenic enrichments and diagenetic modifications. Absolute concentrations determined by two methods, x-ray fluorescence and acid leaching for bioavailability, are not comparable. However, vertical trends in concentrations of the cored sediment are comparable. To assess levels of anthropogenic pollution, enrichment factors (enriched concentrations in upper core divided by background levels in lower core) are preferred over index of accumulation (I geo) values because preindustrial or background levels of heavy metals are well constrained. The ten metals are placed into three groups: (1) Cu, Pb, and Zn, which show the most anthropogenic enrichment; (2) As, Cd, Cr, Ni, and Sb, which are often associated with anthropogenic pollution but show only minor enrichment; and (3) Fe and Mn, which are diagenetically enriched. Assuming harbor waters are well mixed, anthropogenic enrichments of Cu, Pb, and Zn, are time correlative, but the degree of enrichment depends on the method of analysis and core location. Levels of As, Cd, Pb, and Zn show small variations in preindustrial sediments that are not related to changes in grain size and probably result from changes in the oxidation-reduction potential of the sediments and salinity of the pore waters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00770603
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Mechanisms mediating insulin-induced hypotension in rats (1996)
    Springer
    Acta diabetologica 33 (1996), S. 263-268 
    Details
    ISSN: 1432-5233
    Keywords: Insulin-induced hypotension ; Adrenergic antagonists ; Ganglionic blockers ; Cholinergic antagonist ; Atropine ; Hexamethonium ; Prazosin ; Atenolol ; L-NAME ; Nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms associated with insulin-induced cardiovascular inhibitory responses were evaluated in untreated normal rats and in normal rats pretreated with an antagonist of nitric oxide (NO) production (L-NAME), with cholinergic, alpha- and beta-adrenergic antagonists, or after ganglionic blockade. Male Wistar rats were anesthetized with a mixture of urethane and alpha-chloralose and placed on a electric heating pad. The femoral artery and vein were cannulated for measurements of mean arterial pressure (MAP), heart rate, plasma glucose, blood sampling, and intravenous injections. Intravenous injection of insulin (5.0 U/kg) in untreated rats resulted in a significant and sustained decrease in arterial blood pressure (average 24%) and in a slight decrease in heart rate. These cardiovascular responses were blocked by L-NAME and by the cholinergic antagonist atropine, suggesting an involvement of NO and the cholinergic receptors, or an effect of insulin on the central nervous system parasympathetic center. The ganglionic blocker hexamethonium attenuated the insulin-induced response. On the other hand, the hypotensive effect of insulin persisted after sympathetic blockade with the alpha-1 antagonist prazosin and the beta-1 antagonist atenolol. We conclude that the insulin-induced decrease in blood pressure is due to both increased cholinergic outflow and to NO production and that an enhanced sympathetic activity possibly mediated by a reactive release of norepinephrine or epinephrine modulates this response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571561
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Mechanisms mediating insulin-induced hypotension in rats (1996)
    Springer
    Acta diabetologica 33 (1996), S. 263-268 
    Details
    ISSN: 1432-5233
    Keywords: Key words Insulin-induced hypotension ; Adrenergic antagonists ; Ganglionic blockers ; Cholinergic antagonist ; Atropine ; Hexamethonium ; Prazosin ; Atenolol ; L-NAME ; Nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms associated with insulin-induced cardiovascular inhibitory responses were evaluated in untreated normal rats and in normal rats pretreated with an antagonist of nitric oxide (NO) production (L-NAME), with cholinergic, alpha- and beta-adrenergic antagonists, or after ganglionic blockade. Male Wistar rats were anesthetized with a mixture of urethane and alpha-chloralose and placed on a electric heating pad. The femoral artery and vein were cannulated for measurements of mean arterial pressure (MAP), heart rate, plasma glucose, blood sampling, and intravenous injections. Intravenous injection of insulin (5.0 U/kg) in untreated rats resulted in a significant and sustained decrease in arterial blood pressure (average 24%) and in a slight decrease in heart rate. These cardiovascular responses were blocked by L-NAME and by the cholinergic antagonist atropine, suggesting an involvement of NO and the cholinergic receptors, or an effect of insulin on the central nervous system parasympathetic center. The ganglionic blocker hexamethonium attenuated the insulin-induced response. On the other hand, the hypotensive effect of insulin persisted after sympathetic blockade with the alpha-1 antagonist prazosin and the beta-1 antagonist atenolol. We conclude that the insulin-induced decrease in blood pressure is due to both increased cholinergic outflow and to NO production and that an enhanced sympathetic activity possibly mediated by a reactive release of norepinephrine or epinephrine modulates this response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571561
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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