The Experts below are selected from a list of 30 Experts worldwide ranked by ideXlab platform

K F Austen - One of the best experts on this subject based on the ideXlab platform.

Masaaki Matsuo - One of the best experts on this subject based on the ideXlab platform.

Paul M Obyrne - One of the best experts on this subject based on the ideXlab platform.

  • treatment of asthma with drugs modifying the leukotriene pathway
    The New England Journal of Medicine, 1999
    Co-Authors: Jeffrey M Drazen, Elliot Israel, Paul M Obyrne
    Abstract:

    In 1979 and 1980, the chemical structures of the material previously known as Slow-Reacting Substance of anaphylaxis were elucidated as 5(S)- hydroxy- 6(R)-glutathionyl- 7,9-trans-11,14- cis - eico- satetraenoic acid1 and its cysteinyl-glycyl and cysteinyl congener (also known as leukotrienes C4, D4, and E4, respectively). These molecules were so named because the parent molecule was originally isolated from leukocytes, and its carbon backbone contained three double bonds in series, which constitutes a triene. This structural information provided the key to the oxidative pathway of lipid metabolism known as the 5-lipoxygenase pathway. One of . . .

Shinji Shigenaga - One of the best experts on this subject based on the ideXlab platform.

Keigo Nishino - One of the best experts on this subject based on the ideXlab platform.

  • Effect of Ibudilast, a Novel Antiasthmatic Agent, on Anaphylactic Bronchoconstriction: Predominant Involvement of Endogenous Slow Reacting Substance of Anaphylaxis
    International Archives of Allergy and Immunology, 1993
    Co-Authors: Mitsuo Ohashi, Takashi Uno, Keigo Nishino
    Abstract:

    The effect of ibudilast on anaphylactic bronchoconstriction was studied in guinea pigs sensitized actively with ovalbumin (OA). Animals were treated with indomethacin, tripelennamine and propranolol prior to the antigen challenge. Anaphylactic bronchoconstriction was prevented by ibudilast (1–4 mg/kg i.v. and 5–20 mg/kg p.o.) dose-dependently. FPL55712 and phenidone were also effective. Even when administered at the maximum development of bronchoconstriction, ibudilast (0.5 and 2 mg/kg i.v.) and FPL 55712 caused significant reduction of the increased airway tone, while phenidone did not. Ibudilast (1–4 mg/kg i.v.) and FPL55712 inhibited leukotriene D4-induced airway responses in nonsensitized guinea pigs pretreated with indomethacin and propranolol. Ibudilast (1.6 and 4 mg/kg i.v.) inhibited platelet-activating-factor (PAF)-induced airway responses in nonsensitized guinea pigs pretreated with indomethacin and propranolol, however, FPL 55712 inhibited PAF-induced airway responses only at a high dose such as 10 mg/kg i.v. Ibudilast (4 mg/kg i.v.) did not inhibit acetylcholine-induced airway response. Ibudilast showed inhibition of the release of Slow-Reacting Substance of anaphylaxis (SRS-A) from guinea pig chopped lung sensitized with OA, which was significantly diminished by indomethacin. The drug little affected the activity of phospholipase A2 and 5-lipoxygenase in guinea pig polymorphonuclear leukocytes. These results indicate that ibudilast inhibits anaphylactic bronchoconstriction which is considered to be largely mediated by endogenously released SRS-A. The inhibitory effect of ibudilast on anaphylactic bronchoconstriction in the presence of indomethacin is considered to be exerted through its antagonism to SRS-A.