INCREASED NITRIC-OXIDE BIOSYNTHESIS IN LEUKOTOXIN,9,10-EPOXY-12-OCTADECENOATE INJURED LUNG

被引:24
作者
ISHIZAKI, T
SHIGEMORI, K
YAMAMURA, Y
MATSUKAWA, S
NAKAI, T
MIYABO, S
HAYAKAWA, M
OZAWA, T
VOELKEL, NF
机构
[1] CIBA GEIGY AG,INT RES INST,TAKARAZUKA,HYOGO,JAPAN
[2] FUKUI MED SCH,CENT RES LAB,FUKUI 91011,JAPAN
[3] NAGOYA UNIV,DEPT BIOMED CHEM,NAGOYA,AICHI 466,JAPAN
[4] UNIV COLORADO,HLTH SCI CTR,CTR PULMONARY HYPERTENS,DIV PULM & CRIT CARE MED,DENVER,CO 80262
关键词
D O I
10.1006/bbrc.1995.1637
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We measured effluent nitric oxide levels using a chemiluminescence method from leukotoxin (Lx, a linoleate epoxide) injured isolated rat lungs perfused with physiological salt solution. Nitric oxide production from Lx-injured lung promptly increased and lasted for 20 min. Pretreatment with N-G-monomethyl-L-arginine (LNMMA) significantly suppressed Lx-induced production of nitric oxide. Effluent from control lungs showed trace levels of nitric oxide. The wet to dry lung weight (WLW/DLW) after termination of the experiments was significantly elevated in Lx-treated lungs compared with that of LNMMA pretreated lungs or control lungs. There was a correlation between nitric oxide levels (at 10 min) and lung edema (WLW/DLW). Thus, nitric oxide plays a role in the pathogenesis of Lx-induced lung injury. (C) 1995 Academic Press, Inc.
引用
收藏
页码:133 / 137
页数:5
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