We examined the effect of
fudosteine, a
cysteine derivative, on blood flow of tracheal microvasculature increased by airway
inflammation. Airway
inflammation was elicited by
sulfur dioxide (SO(2)) exposure for 2 weeks in rabbits. Each
drug (500 mg/kg, p.o.) or 0.5%
carboxymethylcellulose-Na (control group) was daily administered just before SO(2) exposure. After final SO(2) exposure was finished, blood flow of tracheal microvasculature was measured by blood perfusion monitor.
Fudosteine or
S-carboxymethylcysteine (S-CMC) significantly suppressed blood flow of tracheal microvasculature increased by SO(2) exposure. However, no effect of
fudosteine was observed on the pharmacological microvascular response in trachea of SO(2)-exposed rabbits. On the other hand,
fudosteine or S-CMC scavenged
superoxide anion generated from rat neutrophils, and enzymatically generated from
xanthine oxidase-
acetaldehyde reaction. The results suggest that suppressive action in increased tracheal blood flow of
fudosteine is due to anti-inflammatory activity, at least in part, via scavenging of
superoxide anion.