Measurement of SRS-A activities in plasma of asthmatic patients.

Ohtsu, Hiroshi; Mue, Suetsugu; Tamura, Gen; Yamauchi, Kohei; Ishihara, Toshiharu; Sato, K.; Takishima, Tamotsu

doi:10.1620/tjem.145.197

Cited by 5 publications

(2 citation statements)

References 15 publications

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“…Leukotriene release has been detected in plasma by bioassay after antigen challenge of indomethacin-treated and sensitized gui nea pigs [24]. More recent studies in humans have suc cessfully demonstrated changes in leukotriene levels in the blood of asthmatics [33,34]. However, these studies have used large quantities of plasma in the case of the humans or indomethacin treatment in the case of the guinea pigs to obtain detectable quantities of peptidoleukotrienes in plasma.…”

Section: Discussionmentioning

confidence: 99%

Mediators of C5a-Induced Bronchoconstriction in the Guinea Pig

Regal

Bell²

1987

Int Arch Allergy Immunol

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The effect of intravenous injection of C5a on pulmonary resistance and dynamic lung compliance was determined in anesthetized, artificially respirated guinea pigs. A mixture of C5a plus C5a_{des arg} was purified from yeast-activated guinea pig serum and is referred to as C5a. Intravenous injection of C5a caused a dose-related bronchoconstriction as evidenced by a decrease in compliance and increase in resistance. Conversion of the C5a in the mixture to C5a_{des arg} by carboxypeptidase B digestion did not significantly alter the magnitude of the bronchoconstriction. Pharmacological antagonists were employed to determine if histamine, acetylcholine or products of the arachidonate metabolism were mediators of C5a-induced bronchoconstriction. The histamine H₁ antagonist pyrilamine inhibited the C5a-induced bronchoconstriction, suggesting the involvement of histamine. The cholinergic receptor antagonist atropine in combination with pyrilamine caused an inhibition of the C5a-induced increase in resistance but not compliance, suggesting acetylcholine does not play a major role in C5a-induced bronchoconstriction beyond its known role in participating in histamine-induced bronchoconstriction. Involvement of arachidonate metabolites was suggested by the ability of the cyclooxygenase inhibitor, indomethacin, to prevent the C5a-induced bronchoconstriction. Because indomethacin also caused a delay in the leukotriene C₄ (LTC₄)-induced bronchoconstriction, the participation of peptidoleukotrienes in the C5a-induced bronchoconstriction could not be ruled out. The leukotriene antagonists FPL 55712 and L-649,923 were evaluated for their specificity in inhibiting LTC₄-induced bronchoconstriction. FPL 55712 was nonselective since it inhibited prostaglandin D₂ and histamine-induced bronchoconstriction as well as LTC₄-induced bronchoconstriction. L-649,923 inhibited only the LTC₄-induced bronchoconstriction and was without effect on the C5a-induced bronchoconstriction, suggesting that peptidoleukotrienes are not important mediators of C5a-induced bronchoconstriction. Using radioimmunoassay, the change in peptidoleukotriene levels detected in plasma during C5a-induced bronchoconstriction was not significantly different from 0. Thus, these studies have quantitated the C5a-induced decrease in dynamic lung compliance and increase in pulmonary resistance and suggest that histamine and cyclooxygenase products, but not peptidoleukotrienes, play a major role in C5a-induced bronchoconstriction.

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Section: Discussionmentioning

confidence: 99%

Mediators of C5a-Induced Bronchoconstriction in the Guinea Pig

Regal

Bell²

1987

Int Arch Allergy Immunol

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“…The cysteinyl leukotrienes are potent airway contrac‐ tile agonists 1–4 that are known to be produced by eosinophils 5–7 and mast cells. 8 They can be recovered from body fluids of patients with asthma during induced 9,10 or spontaneous 11,12 asthma attacks. Cysteinyl leukotriene receptor antagonists have been reported to cause significant inhibition of cold air‐, 13 exercise‐, 14,15 allergen‐ 16–18 and aspirin‐induced 19–21 asthma.…”

Section: Introductionmentioning

confidence: 99%

Population-based open-label clinical effectiveness assessment of the cysteinyl leukotriene receptor antagonist pranlukast

Tamura

Inoue

Chihara

et al. 2000

Allergology International

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Although the efficacy of cysteinyl leukotriene receptor antagonists in asthma therapy has been established through controlled clinical trials, there are no data concerning the effectiveness of their use in clinical practice, in which there is no rigid selection based on specific inclusion and exclusion criteria. The aim of the present study was to evaluate the effectiveness of pranlukast in clinical practice. More than 2500 outpatients with mild to severe persistent asthma answered an input questionnaire, which consisted of 33 items assessing asthma symptoms in terms of six activities of daily living during the previous 2 weeks. Of these patients, 1138 received treatment with pranlukast and answered the same questionnaire 4–6 weeks after the start of treatment. In 923 of these 1138 patients, we examined the impact of concomitantly used inhaled steroids, β2‐adrenergic agonists or sustained‐release theophylline on the effectiveness of pranlukast treatment. One hundred and sixty‐seven control patients completed the questionnaire twice but did not receive pranlukast treatment. We found a significant decrease in the number of asthma symptoms reported among both the 1138 patients treated with pranlukast and the 167 control patients. However, the magnitude of the decrease in symptoms was significantly (P < 0.001) greater with pranlukast treatment. Moreover, pranlukast was equally efficacious in the presence and absence of concomitantly used inhaled steroids, β2‐adrenergic agonists or sustained‐release theophylline. In conclusion, pranlukast was shown to have clinical effective‐ ness in the treatment of mild to severe persistent asthma symptoms.

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Lipoxygenases

Khn¹

1999

Prostaglandins, Laukotrienes and Other Eicosanoids

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Measurement of SRS-A activities in plasma of asthmatic patients.

Cited by 5 publications

References 15 publications

Mediators of C5a-Induced Bronchoconstriction in the Guinea Pig

Mediators of C5a-Induced Bronchoconstriction in the Guinea Pig

Population-based open-label clinical effectiveness assessment of the cysteinyl leukotriene receptor antagonist pranlukast

Lipoxygenases

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