Disodium cromoglycate and compounds with similar activities

Buckle, Derek R.

doi:10.1016/b978-0-408-11576-6.50018-8

Cited by 6 publications

(2 citation statements)

References 161 publications

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“…Although regarded by many as presumptuous in 1976, the conclusion was not hotly disputed in 1981 and, with the passage of time and the demise of further cromoglycate analogues, has become conventional wisdom. It is interesting to consider why the concept of mast cell stabilisation became so strongly established to the extent that it is still promulgated in academic medicine [15], even though in the pharmaceutical industry these tests have been widely accepted as inappropriate [ 16].…”

Section: Evaluation Of the Mast Cell Conceptmentioning

confidence: 99%

Platelet activating factor and asthma

Morley¹

1986

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First encountersDavid Gordon joined me at the Kennedy Institute of Rheumatology, bringing with him a newly developed radio-immunoassay for E-type prostaglandins (PGs) and an experience of industrial pharmacology. The prospect of having an immunoassay for PGs was especially attractive, for it provided an opportunity to determine whether a particular inflammatory cell population might serve as the major source of E-type PGs in inflammation. At that time, the prevailing and authoritative view was that neutrophils subserved that function [1,2]. However, our examination of the abundant neutrophils that were collected from the synovial effusion from an untreated patient with acute rheumatoid arthritis was unrewarding. Inconsequentual levels of PGs were produced by synovial neutrophils following short term culture, an observation in marked contrast with the substantial amounts of E-type PGs present within the synovial fluid [3]. These results prompted culture of macrophage-rich populations as a control, thereby revealing the production of substantial quantitives of E-type PGs by this cell type [3]. Our conclusions, derived initially from bioassay and radioimmunoassay were confirmed subsequently by definitive chemical techniques [4]. These observations led to the recognition that PGE2 formation by macrophages can regulate lymphokine secretion [5], an interpretation which has survived the vagaries of immunological nomenclature [6]. My academic bias was to pursue the regulation of lymphokine production, whilst David Gordon favoured use of macrophage cultures for the study of drug effects and he made the novel observation that glucocorticosteroids resembled non-steroidal antiinflammatory drugs by inhibiting PG formation [7]. In addition to introducing me to glucocorticosteroids, these experiments marked my first encounter with the anti-asthma drug cromoglycate. Cromoglycate had been included in these studies, since David Gordon was already (in 1973) aware that the mode of action of this drug in asthma was uncertain; hence, he reasoned that a new pharmacological test might detect a relevant property of cromoglycate. In the event, his observations were negative and this outcome is echoed a decade later in analogous studies of thromboxane formation [8]. However, the idea was not unreasonable and in the interim, it has been reported that lysosomal enzyme release, following IgE-dependent activation of macrophages was reduced by cromoglycate [9]. Cromoglycate and the mast cellDiscovery of cromoglycate was not a consequence of some profound insight into asthma; rather, it resulted from empirical self-medication by Dr. Roger Altounyan. This unconventional approach was vindicated by the detection of a wholly novel substance, that is effective in asthma prophylaxis [10]. In such circumstances, it is proper that pharmacologists must consider whether cromoglycate

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Section: Evaluation Of the Mast Cell Conceptmentioning

confidence: 99%

Platelet activating factor and asthma

Morley¹

1986

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“…Mast cell stabilization and PAF-induced hyperreactivity: One consequence of the con cept that mast cell activity is central to asthma excabation has been the emergence of a suc cession of compounds which inhibit mast cell activation (27). Tranilast and oxatoride are potent inhibitors of mast cell activation and hence fall into this category.…”

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The effect of prophylactic anti-asthma drugs on PAF-induced airway hyperreactivity.

Sanjar¹,

Smith²,

Schaeublin³

et al. 1989

Jpn.J.Pharmacol

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Abstract-Intravenous injection of platelet activating factor (PAF) in anesthetized guinea pigs induces non-selective airway hyperreactivity. This response to PAF was reduced in a dose-dependent manner by systemic administration of established prophylactic anti-asthma drugs (ketotifen, cromoglycate, aminophylline and gluco corticosteroids) and by competitive antagonists of PAF. These inhibitory effects could not be accounted for by antagonism of histamine (H1), serotonin or peptido leukotrienes receptors; parasympatholytic activity; cyclo-oxygenase or lipoxy genase inhibition; mast cell stabilization; or bronchodilatation.Infusion or injection of PAF to induce airway hyperreactivity in the guinea pig may provide a prospective test for prophylactic anti-asthma drugs.

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