Takamura Muraki (1), Emiko Fujii (1), Midori Okada (2), Hiroaki Horikawa (2), Kaoru Irie (1) and Ken-ichi Ohba (1)
(1) Department of Pharmacology and (2) Department of Chemistry, Tokyo Women's Medical College, Kawada-cho 8-1, Shinjuku-ku, Tokyo 162, Japan
Abstract: By dye leakage in mouse skin, we evaluated the inhibition of proinflammatory stimuli-induced plasma extravasation by a putative inhibitor of inducible nitric oxide synthase, S-ethylisothiourea. A low dose of S-ethylisothiourea (5 microg/kg) mimicked aminoguanidine in inhibiting the plasma extravasation elicited by lipopolysaccharide but not by 5-hydroxytryptamine or platelet-activating factor. A higher dose of S-ethylisothiourea (10 microg/kg) inhibited the plasma extravasation induced by 5-hydroxytryptamine slightly; however, it increased the basal dye leakage. Thus, S-ethylisothiourea may be used as a relatively specific inhibitor for inducible nitric oxide synthase in vivo.
Vascular permeability, Inducible nitric oxide synthase, Lipopolysaccharide
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