흰쥐 비점막에서 혈장의 혈액외유출에 대한 산화 질소의 역할

초록

Background and Objectives：Platelet-activating factor (PAF), a potent chemical mediator in inflammation and allergic reaction, induces microvascular leakage in several tissues. In rat airways, the PAF-induced microvascular leakage is not dependent on cyclooxygenase or lipoxygenase products nor on circulating platelets, and it is probably mediated by receptors on the vascular endothelium. Nitric oxide (NO), first identified as endothelium-derived relaxing factor, has been recently reported to be an important mediator of the neurogenic vascular exudative process. The aim of this study was to investigate the role of NO in the PAF-induced microvascular leakage in rat nasal and tracheal mucosa. Methods：PAF (1 μg/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 μg/mg wet tissue, respectively, and those of the L-NAME pretreated rats were 6.643 and 6.987 μg/mg wet tissue, respectively. Tissue sections of the L-NAME pretreated rats showed a definitely decreased extravasation of Evans blue under the fluorescence microscopy. Conclusion：Pretreatment with L-NAME clearly inhibited the PAF-induced microvascular leakage in the nasal and tracheal mucosa of rat. This finding also implies that NO may mediate the PAF-induced microvascular leakage in rat airways.

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