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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of chemical & engineering data 6 (1961), S. 557-560 
    ISSN: 1520-5134
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 17 (1986), S. 466-471 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Formyl-methionyl-leucyl-phenylalanine (FMLP) is a synthetic acylated oligopeptide related to chemotactic peptides released by bacteria. In order to determine whether FMLP causes bronchoconstrictionin vivo, we studied the effects of neubulized FMLP on lung resistance (RL) in the rabbit. In fourteen rabbits baseline RL was measured and then dimethylsulfoxide (DMSO) alone and 0.3, 1, 3 and 10 mg/ml FMLP in DMSO was nebulized and inhaled by the rabbits over periods of 2 min each. After each concentration the RL was re-measured and the results expressed as a % of the RL following DMSO alone. In 6 rabbits the response to serial nebulization of DMSO alone was 5.5±10.4% (mean±2 SD). In 8 rabbits receiving FMLP there was a dose dependent increase in RL of 20% or greater whereas 6 rabbits failed to respond. Since there are known receptors for FMLP on neutrophils, 10 further rabbits were rendered neutropenic using nitrogen mustard and the studied as above. Eight of these rabbits failed to respond significatly to FMLP whereas 2 had a 20% or greater increase in RL. In each bronchial specimen from 6 additional rabbits FMLP failed to induce airway contractionin vitro. We conclude that FMLP causes a variable degree of bronchoconstriction in rabbits, that this response may, in part, be mediated via the neutrophil and is unlikely to be due to direct smooth muscle contraction.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 12 (1985), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Airway preparations from the trachea, main bronchi, subsegmental bronchi and the parenchyma of rabbits were studied.2. The proximal airways, the trachea and main bronchi, were less sensitive to histamine than the distal airways of the subsegmental bronchi and lung parenchymal strip.3. The proximal airways were more sensitive to carbachol than the distal airways.4. These results may assist in the interpretation of airway responses in vivo.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 14 (1987), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The mechanism of C5a des Arg-induced airway hyper-responsiveness in rabbits was investigated.2. Airway smooth muscle from rabbits which had been pretreated in vivo, was studied in vitro. Tracheal rings, segmental bronchial rings, subsegmental bronchial spirals and lung parenchymal strips were all prepared from each rabbit lung.3. Although C5a des Arg produces hyper-responsiveness to histamine in vivo, which is inhibited by indomethacin, the airway smooth muscle responses in vitro from control, C5a des Arg and C5a des Arg plus indomethacin pretreated rabbits did not differ.4. The neutrophil counts in the tracheal and subsegmental bronchial specimens were increased in the C5a des Arg-treated group. Indomethacin significantly (P〈0.05) inhibited the neutrophil influx in the subsegmental bronchi.5. It is concluded that intrinsic smooth muscle function is unaltered following C5a des Arg-induced hyper-responsiveness in vivo.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 11 (1984), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The antagonist effects of indoramin were investigated in rabbit perfused ear artery, common carotid artery, and human perfused temporal artery preparations.2. Indoramin was a potent competitive antagonist of the constrictor effects of noradrenaline (NA) in all three preparations, pA2 values being 7.77 for the ear artery, 8.20 for the common carotid artery and 7.46 for the human temporal artery.3. The constrictor actions of serotonin (5-hydroxytryptamine, 5-HT) were competitively antagonized by indoramin. The pA2 values obtained in the rabbit common carotid and human temporal artery (5.92 and 6.25, respectively), were lower than those for NA in the same preparations and lower than that obtained in the rabbit perfused ear artery (7.55).4. Indoramin was a potent competitive antagonist (pA2:8.31) of histamine-induced vasoconstriction in the rabbit perfused ear artery preparation.5. These results can be explained on the basis of previous findings that the action of 5-HT in the rabbit ear artery is mediated via an α-adrenoceptor, and that the rabbit common carotid artery contains true 5-HT receptors. The findings suggest that specific 5-HT receptors may be present in the human temporal artery and that α-adrenoceptor antagonism may be the pharmacological property of most relevance to the efficacy of indoramin in migraine prophylaxis.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 23 (1993), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although it has been postulated that inflammatory cells cause the bronchial hyper-responsiveness which is diagnostic of asthma [1], until recently there has been little direct evidence of such a link. We have recently shown that calcium ionophore-activated human neutrophils and eosinophils can induce a state of human airway hyperresponsiveness in vitro [2]. In this study we have shown that the anti-inflammatory agent nedocromil sodium, 10-7m, inhibited the hyperresponsiveness induced by products released from ionophore activated neutrophils but did not inhibit the release of leukotriene B4 from the same cells. Neutrophil-induced bronchial hyperresponsiveness was also inhibited by pre-treatment of the bronchial tissues with a thromboxane A2 and prostaglandin receptor antagonist, GR32191,10-7m. These findings indicate that cyclooxygenase products are involved in bronchial hyperresponsiveness induced by inflammatory cell products in vitro and that their release can be inhibited by nedocromil sodium.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 26 (1996), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The two main features of asthtna are bronchial hyperresponsiveness and inflammation. The inflammatory response in asthma consists of infiltration and activation of a variety of inflammatory cells including neutrophils. Our previous studies have shown that stimuhited neutrophil supernatants cause hyperresponsiveness of human bronchial tissue in vitro.Objective To investigate the effect of the sensitization status of the tissue and the albumin concentration used to prepare supernatants on the response of human bronchial tissue to stimulated neutrophil supernatants.Methods Neutrophil supernatants were prepared from human isolated blood in the presence of varying concentrations of albumin (0%, 0.1% and 4%), Neutrophil supernatants were added to sensitized and non-sensitized human isolated bronchial tissue which was stimulated with electrical field stimulation (EFS) (20 s every 4min). Receptor antagonists specific for the prostaglandin and thromboxane (10−7M GR3219I), platelet activating factor (10−6M WEB 2086), leukotriene D4 (10−6M MK-679) and neurokinin A (10−7M SR48968) receptors were used to identify neutrophil products responsible for the effects observed in the bronchial tissue. Results In non-sensitized human bronchial tissue, stimulated neutrophil supernatants induced a direct contraction in the presence of 0% and 0.1 % but not 4% albumin. This contraction was due to leukotriene D4 as MK-679 completely inhibited the contraction. In contrast, stimulated neutrophil supernatants increased responsiveness of sensitized human bronchial tissue to EFS. The increased responsiveness was observed only in the presence of 0.1% albumin, with the site of modulation likely to be prejunctional on the parasympathetic nerve. The increased responsiveness was not inhibited by any of the antagonists tested.Conclusion Sensitization status of the tissue and albumin concentration effect the responsiveness of human bronchial tissue to stimulated neutrophil supernatant. Our results suggest a possible role for neutrophils in hyperresponsiveness.
    Type of Medium: Electronic Resource
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  • 8
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    Saskatoon : Periodicals Archive Online (PAO)
    Canadian journal of history/Annales canadiennes d'histoire. 26:2 (1991:Aug./août) 352 
    ISSN: 0008-4107
    Topics: History , Economics
    Description / Table of Contents: Modern Europe
    Notes: Reviews
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  • 9
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    Unknown
    Saskatoon : Periodicals Archive Online (PAO)
    Canadian journal of history/Annales canadiennes d'histoire. 13:2 (1978:Aug.) 306 
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  • 10
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    Unknown
    Saskatoon : Periodicals Archive Online (PAO)
    Canadian journal of history/Annales canadiennes d'histoire. 16:1 (1981:Apr.) 135 
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