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Titolo:
AIRWAY HYPERRESPONSIVENESS TO ACETYLCHOLINE-INDUCED BY AEROSOLIZED ARACHIDONIC-ACID METABOLITES IN GUINEA-PIGS
Autore:
SATO T; IWAMA T; SHIKADA K; TANAKA S;
Indirizzi:
NISSAN CHEM IND CO LTD,SHIRAOKA RES STN BIOL SCI,1470 SHIRAOKA MINAMISAITAMA SAITAMA 34920 JAPAN NISSAN CHEM IND CO LTD,SHIRAOKA RES STN BIOL SCI MINAMI SAITAMA SAITAMA 34920 JAPAN
Titolo Testata:
Clinical and experimental allergy
fascicolo: 8, volume: 26, anno: 1996,
pagine: 957 - 963
SICI:
0954-7894(1996)26:8<957:AHTABA>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
HISTAMINE HYPERRESPONSIVENESS; INHALED LEUKOTRIENE-D4; SMOOTH-MUSCLE; REACTIVITY; RESPONSIVENESS; ASTHMA; PGD2; METHACHOLINE; ANTAGONIST; MEDIATORS;
Keywords:
ARACHIDONIC ACID METABOLITES; AIRWAY HYPERRESPONSIVENESS; GUINEA-PIGS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
T. Sato et al., "AIRWAY HYPERRESPONSIVENESS TO ACETYLCHOLINE-INDUCED BY AEROSOLIZED ARACHIDONIC-ACID METABOLITES IN GUINEA-PIGS", Clinical and experimental allergy, 26(8), 1996, pp. 957-963

Abstract

Background and objective To investigate the role of arachidonic acid (AA) metabolites in airway hypersensitivity. Method We studied the change in airway responsiveness to acetylcholine (ACh) after inhalation of some AA metabolites in guinea-pigs. Results Exposure to prostaglandin (PG) D-2, thromboxane (TX) A(2) mimetic U-46619, leukotriene (LT) D-4 or LTE(4) at concentrations which did not influence bronchial tone and blood pressure dose-dependently caused airway hyperresponsiveness. However,. the change was not observed after challenge with a high concentration of PGF(2 alpha). Furthermore, PGD(2) and U-46619 induced an acute and short-lived increase in responsiveness, while LTD(4) and LTE(4) induced a slow-onset and longer-lived increase. In the tachyphylaxis study, although the tachyphylaxis for airway hyperresponsiveness provoked by PGD(2) and U-46619 was not observed, airway hyperresponsiveness induced by the second LTD(4) tended to decrease, and the second LTE(4)-induced airway hyperresponsiveness obviously diminished. In the study using antagonists and inhibitors, TX-receptor antagonist BM-13177inhibited PGD(2)- and U-46619-, but not LTD(4)- and LTE(4)-induced airway hyperresponsiveness. TX synthase inhibitor OKY-046 had no effect on PGD(2)-, U-46619- and LTD(4)-induced airway hyperresponsiveness, while LTE(4)-induced airway hyperresponsiveness tended to be inhibited by these inhibitors. However, the LT-receptor antagonist ONO-1078 inhibited both LTD(4)- and LTE(4)-, but not PGD(2)- or U-46619-induced airway hyperresponsiveness. 5-lipoxygenase inhibitor AA-861 tended to prevent LTE(4)-induced airway hyperresponsiveness, but had no effect on PGD(2)-, U-46619- and LTD(4)-induced enhanced responses. Conclusion These findings indicate that the local existence of PGD(2), TXA(2), LTD(4)and LTE(4) in the guinea-pig airway may act as an airway hyperresponsiveness- inducing factor rather than as a bronchoconstrictor. In addition, PGD(2)/U-46619 may stimulate the TX receptor to induce an acute and short-lived airway hyperresponsiveness, and LTD(4) and LTE(4), which may involve secondary mediator release, may act at the LT receptor to induce a slow-onset and longer-lived airway hyperresponsiveness, which may be associated with the induction, the development and the long duration of airway hyperreactivity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 12:09:41