Dilatory effect of furosemide on rat tracheal arterioles and venules.
Dilatory effect of furosemide on rat tracheal arterioles and venules.
复制标题
呋塞米对大鼠气管小动脉和小静脉的扩张作用。
DOI：
10.1164/ajrccm.156.2.9609123
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Taylor,AE
中科院分区：
文献类型：
--
作者：
Corboz,MR;Ballard,ST;Inglis,SK;Taylor,AE
呋塞米预处理大大降低了对几种类型的支气管收缩剂激发的哮喘反应的严重程度。间接证据表明，速尿通过在热应激期间扩张气道脉管系统来发挥其保护作用。为了检验呋塞米扩张气道微血管的假设，通过手术暴露麻醉大鼠的气管，并持续用加热至37℃的克雷布斯林格碳酸氢盐进行灌注。气管外膜小动脉（初始直径13.0至41.0μm，n = 47）和小静脉（初始直径50.0至99.0μm，n = 46）用视频显微镜观察，并使用视频卡尺测量血管直径。当血管用 10−4M 去氧肾上腺素（一种选择性 α1 肾上腺素能激动剂）预收缩，然后用 10−4M 呋塞米治疗时，在小动脉（从其初始直径的 64.6% 至 79.5%）和小静脉（从其初始直径的 52.1% 至 65.4%）观察到显着（p < 0.05）扩张。当用10−4去氧肾上腺素预收缩血管时，在用环氧合酶抑制剂吲哚美辛（5.0 mg/kg）预处理后，10−4M呋塞米显着扩张小动脉（从其初始直径的77.5％至93.0％）和小静脉（从其初始直径的58.5％至80.1％）。在用一氧化氮合成抑制剂 10−3Ml-NAME 预收缩的血管中，向灌注液中添加 10−4M 呋塞米仍会导致小动脉显着扩张，从其初始直径的 77.4% 扩张至 88.8%，而小静脉则从其初始直径的 79.5% 扩张至 86.7%。这些数据证实，局部应用呋塞米时，通过环氧合酶和一氧化氮独立机制扩张气管小动脉和小静脉。
Furosemide pretreatment greatly reduces the severity of an asthmatic response to several types of bronchoconstrictor challenge. Indirect evidence suggests that furosemide exerts its protective effects by dilating the airway vasculature during thermal stress. To test the hypothesis that furosemide dilates airway microvessels, the tracheas of anesthetized rats were surgically exposed and continuously suffused with Krebs Ringer bicarbonate warmed to 37 ° C. Tracheal adventitial arterioles (13.0 to 41.0 μ m initial diameter, n = 47) and venules (50.0 to 99.0 μ m initial diameter, n = 46) were visualized with a videomicroscope, and vessel diameters were measured using videocalipers. When vessels were preconstricted with 10−4M phenylephrine, a selective α1-adrenergic agonist, and then treated with 10−4M furosemide, significant (p < 0.05) dilation was observed in both arterioles (from 64.6 to 79.5% of their initial diameter) and venules (from 52.1 to 65.4% of their initial diameter). When vessels were preconstricted with 10−4phenylephrine, after pretreatment with the cyclooxygenase inhibitor indomethacin (5.0 mg/kg), 10−4M furosemide significantly dilated arterioles (from 77.5 to 93.0% of their initial diameter) and venules (from 58.5 to 80.1% of their initial diameter). In vessels preconstricted with 10−3Ml-NAME, an inhibitor of nitric oxide synthesis, addition of 10−4M furosemide to the suffusion still caused significant dilation in arterioles, from 77.4 to 88.8% of their initial diameter, and in venules from 79.5 to 86.7% of their initial diameter. These data confirm that furosemide, when applied topically, dilates tracheal arterioles and venules by cyclooxygenase- and nitric oxide- independent mechanisms.