Effect of UV irradiation and rebamipide on the blood flow and viability of rabbit skin flap

ABSTRACT

This study was undertaken to examine the effects of ultraviolet light (UVL) and rebamipide on the cutaneous blood flow and tissue survival on rabbit skin flap. In a random bipedicle flap, Laser Doppler Flowmetry (LDF) was employed to measure the blood flow of flap (BFF). Wound Margin Strength (WMS) measured by force transducer and Light microscopy were used for evaluation of tissue viability. Single exposure to UVL increased the BFF gradually for more than 15 hours, and decreased the vasoconstrictor effect of intravenous phenylephrine. The UVL-induced increase in BFF regressed after 18 hours of irradiation, and this regression was tended to be enhanced by intradermal injection of L-NAME, a nitric oxide synthase (NOS) inhibitor, but the regression was significantly reversed by acetylcholine, an endothelial constitutive NOS (cNOS) activator and L-arginine, an NO precursor. Rebamipide, a novel antiulcer oxide synthase (NOS) inhibitor, but the regression was significantly reversed by acetylcholine, an endoagent known to scavenge the hydroxyl radical, abruptly reversed the spontaneous regression of the UVL-induced increase in BFF by the same manner as L-arginine. In ischemic skin flap, rebamipide increased the BFF abruptly by the same manner as sodium nitroprusside (SNP), an NO doner, while N-acetylcystein (NAC), a free radical scavenger, gradually increase the BFF. The rebamipide-induced increase in BFF was sustained at the level of the SNP-induced increase in BFF during the late period of experiment. Rebamipide increased the WMS of skin flaps and prevented the tissue necrosis in comparison with L-NAME. Based on these results, it is concluded that in rabbit skin, UVL irradiation increases the BFF by NO release, and rebamipide exerts a protective effect on the viability of ischemic skin flaps by either or both the increase in BFF by NO release and free radical scavenger effect.