Effect of fudosteine, a cysteine derivative, on blood flow of tracheal microvasculature increased by airway inflammation

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.