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首页> 外文期刊>Biomedical Research >Nedocromil Sodium Inhibits Hypertonic Saline-induced Plasma Extravasation in Guinea Pig Airways
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Nedocromil Sodium Inhibits Hypertonic Saline-induced Plasma Extravasation in Guinea Pig Airways

机译：奈多克罗米钠抑制豚鼠气道高渗盐引起的血浆外渗。

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We investigated the potential of nedocromil sodium (NS) to reduce neurogenic plasma extravasation induced by hypertonic saline in guinea pig airways. Plasma extravasation was assessed by photometric measurement of extravasated Evans blue after formamide extraction. Hypertonic saline was delivered to anesthetized, artificially ventilated guinea pigs through a tracheal cannula. Inhalation of hypertonic saline for 2 min increased Evans blue dye extravasation in the trachea in a concentration-dependent (0.9, 5, 10, 15 and 20%) manner. The increase in plasma extravasation induced by hypertonic saline (15%) was significantly reduced by pretreatment with NS (10 mg/kg, i.v.). The inhibition of plasma extravasation by NS (10 mg/kg, i.v.) alone was not different from the inhibition induced by the combination of NS and the bradykinin B_2 receptor antagonist, HOE140 (0.1 #mu#mol/kg, i.v.) or HOE140 (0.1 #mu#mol/kg, i.v.) alone. However, pretreatment with the combination of NS (10 mg/kg, i.v.) and the tachykinin NK_1 and NK_2 receptor antagonist, FK224 (3.2 mg/kg, i.v.) abolished the increase in plasma extravasation induced by hypertonic saline (15%). The increase in plasma extravasation induced by inhalation of bradykinin (0.1 mM) for 2 min was abolished by pretreatment with NS (10 mg/kg, i.v.). These findings suggest that NS reduced the hypertonic saline-induced plasma extravasation by inhibiting bradykinin-dependent neurogenic inflammation in guinea pig airways.
机译：我们调查了奈多克洛米钠（NS）减少豚鼠气道高渗盐水诱导的神经源性血浆外渗的潜力。通过光度测量甲酰胺提取后外渗的伊文思蓝来评估血浆外渗。高渗盐水通过气管套管输送到麻醉的人工通风的豚鼠。吸入高渗盐水2分钟会以浓度依赖性（0.9％，5％，10％，15％和20％）的方式增加气管中伊文思蓝染料的外渗。用NS预处理（10 mg / kg，i.v.）可明显降低高渗盐水引起的血浆外渗增加（15％）。单独用NS（10 mg / kg，iv）抑制血浆外渗与通过NS和缓激肽B_2受体拮抗剂HOE140（0.1＃mu＃mol / kg，iv）或HOE140（单独为0.1＃mu＃mol / kg，iv）。但是，用NS（10 mg / kg，静脉内）和速激肽NK_1和NK_2受体拮抗剂FK224（3.2 mg / kg，静脉内）联合进行的预处理消除了高渗盐水引起的血浆外渗增加（15％）。用NS（10 mg / kg，i.v.）预处理可消除因吸入缓激肽（0.1 mM）2分钟而引起的血浆外渗增加。这些发现表明，NS通过抑制豚鼠气道中缓激肽依赖性神经源性炎症而减少了高渗盐水诱导的血浆外渗。

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