Nitric Oxide Synthase Inhibitor Inhibits Platelet Activating Factor: Induced Microvascular Leakage in Rat Nasal and Tracheal Mucosa / 대한이비인후과학회지

ABSTRACT

BACKGROUND AND OBJECTIVE: Platelet-activating factor (PAF), a potent chemical mediator in inflammation and allergic reaction, induces microvascular leakage in several tissues. In rat airways, PAF-induced microvascular leakage is not dependent on cyclooxygenase or lipoxygenase products nor on circulating platelets, and it is probably mediated by receptors on vascular endothelium. Nitric oxide (NO), first identified as endothelium-derived relaxing factor, has been reported recently to be an important mediator of the neurogenic vascular exudative process. The aim of this study was to investigate the role of NO in PAF-induced microvascular leakage in rat nasal and tracheal mucosa. METHODS: PAF (1 ug/kg) was injected intravenously to induce microvascular leakage. The degree of microvascular leakage was measured with the amount of extravasated Evans blue (30 mg/kg) using both spectrophotometry and fluorescence microscopy. Five Sprague-Dawley rats were pretreated with Nw-nitro-L -arginine methyl ester (L-NAME, 10 mg/kg, intravenously, 1 hour before the injection of PAF) to inhibit the NO synthase, while four control rats(n=4) were pretreated with normal saline. RESULT: The average amounts of extravasated Evans blue in the nasal mucosa and trachea of the control rats were 24.789 and 28.238 ug/mg wet tissue, and those of the L-NAME pretreated rats were 6.643 and 6.987 ug/mg wet tissue respectively. Tissue sections of the L-NAME pretreated rats showed a definitely decreased extravasation of Evans blue under fluorescence microscopy. CONCLUSION: Pretreatment with L-NAME clearly inhibited PAF-induced microvascular leakage in the nasal and tracheal mucosa of rat. This finding implies that NO may mediate PAF-induced microvascular leakage in rat airways.