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Effects of an endogenous nitric oxide synthase inhibitor on phorbol myristate acetate‐induced acute lung injury in rats
Author(s) -
Lin Hen I,
Chu Shi Jye,
Wang David,
Chen Hsing I,
Hsu Kang
Publication year - 2003
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2003.03848.x
Subject(s) - bronchoalveolar lavage , lung , nitric oxide synthase , endogeny , nitric oxide , phorbol , chemistry , medicine , endocrinology , arginine , pharmacology , biochemistry , protein kinase c , enzyme , amino acid
Summary 1. In the present study, we determined whether the endogenous nitric oxide (NO) synthase (NOS) inhibitor N ω ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME) could ameliorate the acute lung injury (ALI) induced by phorbol myristate acetate (PMA) in rat isolated lung. 2. Typical ALI was induced successfully by PMA during 60 min of observation. At 2 µg/kg, PMA elicited a significant increase in microvascular permeability (measured using the capillary filtration coefficient K fc ), lung weight gain, lung weight/bodyweight ratio, pulmonary arterial pressure (PAP) and protein concentration of bronchoalveolar lavage fluid. 3. Pretreatment with the NOS inhibitor l ‐NAME (5 mmol/L) significantly attenuated ALI. None of the parameters reflective of lung injury showed significant increase, except for PAP ( P < 0.001). The addition of l ‐arginine (4 mmol/L) blocked the protective effective of l ‐NAME. Pretreatment with l ‐arginine exacerbated PMA‐induced lung injury. 4. These data suggest that l ‐NAME significantly ameliorates ALI induced by PMA in rats, indicating that endogenous NO plays a key role in the development of lung oedema in PMA‐induced lung injury.