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  • 1
    Electronic Resource
    Electronic Resource
    Effect of nifedipine monotherapy on platelet aggregation in patients with untreated essential hypertension (1990)
    Springer
    European journal of clinical pharmacology 39 (1990), S. 403-404 
    Details
    ISSN: 1432-1041
    Keywords: nifedipine ; hypertension ; lipids ; platelet aggregation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of 6 weeks of nifedipine 30–60 mg/d on platelet aggregation and lipid parameters has been studied. A diminution in ADP-, adrenaline- and collagen-induced aggregation was observed. In the case of adrenaline-and collagen-stimulated aggregation the decrease was statistically significant. It was found that platelets which aggregated markedly during the placebo treatment were most strongly inhibited by nifedipine. The changes in lipid parameters were not significantly correlated with changes in aggregation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00315419
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  • 2
    Electronic Resource
    Electronic Resource
    Intranasal challenge with aspirin induces cell influx and activation of eosinophils and mast cells in nasal secretions of ASA-sensitive patients (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 26 (1996), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Although the mechanism of aspirin-sensitivity seems to be related to inhibition of cyclo-oxygenase by aspirin (ASA), the chain of biochemical events leading to the ASA-induced adverse reaction is not clear, and the contribution of particular mediators and inflammatory cells has not been elucidated.Objectives To investigate the involvement of secretory, vascular and cellular mechanisms in the pathophysiology of nasal reactions to aspirin.Methods Six patients with ASA-sensitive asthma/rhinosinusitis and seven ASA-tolerant patients were challenged intranasaly with saline and lysine-acetylsalicylic acid (Lys-ASA) 12mg, on separate occasions. Nasal lavages were obtained before, and then every 15min after challenges, and analysed for biochemical and cellular composition.Results Lys-ASA challenge caused rhinorrhoea. sneezing and nasal congestion with parallel increases in total protein and albumin concentration, albumin % and lysozyme activity in the nasal secretions of ASA-sensitive patients. Concomitant with clinical symptoms, an influx of leucocytes into nasal secretions occurred with significant enrichment in eosinophils (mean prechallenge: 24 ± 12%, postsatine 27±9%, postLys-ASA 51 ± 10%; P 〈 0.03). The influx of eosinophils into nasal secretions was associated with a remarkable increase in Eosinophil Cationic Protein (ECP) immunoreactivity in five of six patients (mean 9.3 ± 3.8 μg/L and 140.9 ± 45.8 μg/mL before and after Lys-ASA, respectively). At the peak of ASA-induced symptoms an increase in the tryptase level was also observed in five of six patients (mean prechallenge: 2 ± 0.1 U/L; postLys-ASA 16 ± 5 U/L; P 〈 0.01) suggesting activation of mucosal mast cells. In ASA-tolerant patients Lys-ASA did not induce significant symptoms or changes in the biochemical and cellular composition of nasal secretions.Conclusion The results show that the ASA-induced nasal adverse reaction involves changes in vascular permeability and serous cell secretion. Both activated eosinophils and mast cells may contribute to the pathophysiology of the ASA-induced reaction in the nasal mucosa.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1996.tb00612.x
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  • 3
    Electronic Resource
    Electronic Resource
    Nasal reactivity to capsaicin in patients with seasonal allergic rhinitis during and after the pollen season (1999)
    Copenhagen : Blackwell Publishing Ltd
    Allergy 54 (1999), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: We aimed to study the participation of neurogenic mechanisms in nasal allergic inflammation by assessing the effect of neurogenic stimulation on the secretory and cellular responses of nasal mucosa in patients with allergic rhinitis. Methods: A group of patients suffering from seasonal allergic rhinitis was challenged intranasally with incremental doses of capsaicin (0.3, 3, 12 μg) during and after the pollen season. Clinical symptoms after provocations were monitored, and unilateral nasal lavages were obtained. The nasal lavage fluid (NAL) was assayed for concentration of total protein, albumin, lactoferrin, and number of leukocytes, following by differential count. Results: Capsaicin challenge during the pollen season produced greater congestion (P〈0.01) and rhinorrhea (P〈0.05) than after the season. The intensity of burning sensation (pain) was similar on both occasions. Capsaicin failed to increase albumin content in NAL both during and after the season. Total protein was increased only after the highest dose of capsaicin (P〈0.03) after the season. The number of eosinophils in basal lavages was higher during the season. During the season, the total number of leukocytes at least doubled in 7/12 patients and the percentage of eosinophils increased in 6/12 patients after the capsaicin challenge. Conclusions: Our study demonstrated that during the symptomatic period the nasal mucosa of allergic patients is more susceptible to neurogenic stimulation, showing enhanced secretory and inflammatory (cellular) responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.1999.00897.x
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  • 4
    Electronic Resource
    Electronic Resource
    Neutrophil chemotactic activity (NCA) in nasal secretions from atopic and nonatopic subjects (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 48 (1993), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In order to elucidate the mechanism responsible for infiltration of nasal mucosa by granulocytes, we tested neutrophil chemotactic activity (NCA) in nasal lavages, by the modified Boyden chamber method, in 16 patients with perennial allergic rhinitis (AR), six ASA-sensitive patients with chronic rhinosinusitis (CRS), and seven normal, nonatopic control subjects (NC). Nasal secretions from all three groups showed significant NCA (mean 157.1±54.0, 62.2±20.7, and 39.4 ± 11.4% of FMLP chemotactic activity for AR, CRS, and NC subjects, respectively). Nasal secretions from patients with AR expressed significantly higher NCA (P〈0.02) than did secretions from NA patients.NCA was unchanged by heating at 56°C for 60 min and was not susceptible to degradation by trypsin. Nasal challenge with Dermatophagoides pteronyssinus antigen induced clinical symptoms and resulted in significant increases in total protein and albumin concentrations in nasal lavages in AR patients, but failed to change the mean NCA activity for up to 40 min after the challenge. These results indicate that nasal secretions from both atopic and nonatopic patients express NCA, but its relation to allergic inflammation remains to be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1993.tb00738.x
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  • 5
    Electronic Resource
    Electronic Resource
    Evaluation of Cerebrospinal Fluid for the Presence of Anticardiolipin Antibodies (aCL) in NP-SLE Patients (2000)
    Springer
    Clinical rheumatology 19 (2000), S. 306-310 
    Details
    ISSN: 1434-9949
    Keywords: Key words:aCL – Cerebrospinal fluid – Systemic lupus erythematosus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Many neurological or psychiatric manifestations of SLE (NP-SLE) are related to the presence of anticardiolipin antibodies (aCL) in the patient’s sera. The aim of this study was to evaluate the presence of aCL in cerebrospinal fluid (CSF) in SLE patients with NP features. Fifteen SLE patients were studied, all with NP features. CSF was evaluated for intrathecal IgG synthesis, oligoclonal IgG, and blood–brain barrier impairment. Sera and CSF were tested by ELISA for the presence of aCL-IgG and aCL-IgM with and without β2 glycoprotein (β2 GPI) cofactor. CSF and sera of 50 low back pain patients served as controls. Six patients were aCL(+) and nine aCL(–). In all patients the general CSF examination was normal. In all patients the value of indices of intrathecal IgG synthesis were normal but oligoclonal protein was present in the CSF of three patients. In none of the patients was the blood–brain barrier impaired. Neither aCL-IgG nor aCL-IgM was detected in the CSF of any NP-SLE patient. Mean levels of aCL in patients without cofactor β2 GPI and with cofactor were as follows: for IgG class 0.005 and 0.057 OD (negative); for IgM class 0.004 and 0.024 OD (negative). We could not detect aCL in the CSF of patients with NP-SLE, even if sera were positive for aCL.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100670070051
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