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  • 1
    ISSN: 1432-1459
    Keywords: Key words Systemic lupus ; erythematosus ; Central nervous ; system ; Cognitive deficits ; Antineuronal antibodies ; Magnetic ; resonance imaging ; Positron ; emission tomography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) remains difficult to diagnose, particularly since structural abnormalities may not be revealed by magnetic resonance imaging (MRI). Glucose utilisation was measured by positron emission tomography (PET) in 35 SLE patients to detect signs of CNS involvement. The patients were examined by a standardised neurological examination, a battery of tests to evaluate neuropsychological performance and MRI. Antineuronal antibodies were determined to investigate their putative role in CNS involvement in SLE. Twenty patients had distinct neurological (17) and/or psychiatric (3) symptoms. Ten patients had pronounced cognitive impairment. Neurological and cognitive deficits were thus found to be unrelated disorders in SLE. Global glucose utilisation of SLE patients did not differ significantly from that of normal controls, nor were differences found between SLE patients with or without neurological or cognitive abnormalities. On MRI of the brain, the number and size of white matter lesions correlated with the presence of neurological deficits but were unrelated to the severity of cognitive impairment. Within the normal range, lower global glucose utilisation tended towards lower values with increasing number and size of white matter lesions. Patients with lesions larger than 8 mm also showed distinctly increased IgG anticardiolipin antibody titres, whereas measuring antineuronal antibodies did not reveal any relation to the variables investigated. We conclude that the demonstration of CNS lesions by MRI can contribute confirmatory evidence for CNS involvement in SLE, but PET or the presence of antineuronal antibodies adds little if any information beyond that obtained by clinical examination, neuropsychological testing, and MRI.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 317 (1981), S. 86-89 
    ISSN: 1432-1912
    Keywords: Glomerular capillary pressure ; Munich-Wistar rat ; Adenosine ; Ureteral obstruction ; Aortic constriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of acute ureteral obstruction (UO) and reduction of renal artery pressure (AC) on the adenosineinduced renal vasoconstriction was studied in the Munich-Wistar rat. Infusion of adenosine, 0.05 μmol/min · kg body weight, into the thoracic aorta, was associated with a fall of directly measured glomerular capillary pressure (P gc) from 45.2+1.8 to 32.5+1.7 mm Hg, P〈0.001. Elevation of ureter pressure to 39+2 mm Hg abolished the fall of P gc following adenosine infusion, 51.3+1.7 vs. 50.0+1.3 mm Hg, NS. Reduction of renal artery pressure to 70 mm Hg by an aortic clamp above the renal arteries also prevented the fall of P gc due to adenosine, 36.8+0.9 vs. 36.4+1.8 mm Hg, NS. Administration of indometacin (10 mg/kg i.v.) restored the ability of adenosine to reduce P gc in UO from 41.5+1.1 to 25.9+2.6 mm Hg (P〈0.001) and in AC from 34.0+3.4 to 28.2+75.7 mm Hg (P〈0.02). Since previous studies have demonstrated that in UO and AC renal prostaglandin synthesis is enhanced the effects of indometacin suggest that prostaglandins could be antagonistic to the action of adenosine on the kidney. The data show that the renal vasculature becomes insensitive to the vasoconstrictive action of adenosine during elevated ureter pressure and reduced renal artery pressure.
    Type of Medium: Electronic Resource
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