Corboz M R, Ballard S T, Inglis S K, Taylor A E
Department of Physiology, College of Medicine, University of South Alabama, Mobile, USA.
Am J Respir Crit Care Med. 1996 Nov;154(5):1382-6. doi: 10.1164/ajrccm.154.5.8912752.
We previously demonstrated that rat tracheal arterioles and large venules constrict in response to alpha-adrenergic agonists and dilate in response to beta-adrenergic agonists. To further investigate the vasodilatory mechanisms in these vessels, we hypothesized that the vascular tone in the tracheal microcirculation is regulated in part by endogenously released nitric oxide (NO). To test this hypothesis, rat tracheal microvessels were visualized in vivo with a video microscope. The change in diameter af adventitial arteriolar (14.5 to 42.0 microm initial diameter, n = 41) and large venular (50.0 to 100.0 microm initial diameter, n = 41) microvessels following the suffusion of vasoactive drugs was measured with video calipers. Significant constriction was observed in arterioles (to 70.0% of initial diameter) and large venules (to 76.6% of initial diameter) after 20 min of suffusion with L-NAME, an inhibitor of NO synthesis. This constriction was in large part reversed by L-arginine, a biochemical precursor of NO, in arterioles (to 93.2% of initial diameter) and in venules (to 90.8% of initial diameter). The combination of prazosin, a selective alpha1-adrenergic antagonist, and yohimbine, a selective alpha2-adrenergic antagonist, also reduced L-NAME-induced constriction in arterioles (to 87.9% of initial diameter) and in venules (to 85.2% of initial diameter). L-arginine or the combination of prazosin and yohimbine alone did not affect the diameter of tracheal microvessels. These data suggest that NO exerts an important influence on tracheal microvascular tone in rats, and may attenuate alpha-adrenergic constriction in these vessels.
我们之前证明，大鼠气管小动脉和大静脉对α-肾上腺素能激动剂产生收缩反应，对β-肾上腺素能激动剂产生舒张反应。为了进一步研究这些血管中的血管舒张机制，我们假设气管微循环中的血管张力部分受内源性释放的一氧化氮（NO）调节。为了验证这一假设，用视频显微镜在体内观察大鼠气管微血管。用视频卡尺测量血管活性药物灌注后外膜小动脉（初始直径14.5至42.0微米，n = 41）和大静脉（初始直径50.0至100.0微米，n = 41）微血管直径的变化。在用L-NAME（一种NO合成抑制剂）灌注20分钟后，观察到小动脉（收缩至初始直径的70.0%）和大静脉（收缩至初始直径的76.6%）出现显著收缩。在小动脉（恢复至初始直径的93.2%）和静脉（恢复至初始直径的90.8%）中，L-精氨酸（NO的生化前体）在很大程度上逆转了这种收缩。选择性α1-肾上腺素能拮抗剂哌唑嗪和选择性α2-肾上腺素能拮抗剂育亨宾的联合使用也减少了L-NAME诱导的小动脉（收缩至初始直径的87.9%）和静脉（收缩至初始直径的85.2%）收缩。单独使用L-精氨酸或哌唑嗪与育亨宾的组合均未影响气管微血管的直径。这些数据表明，NO对大鼠气管微血管张力有重要影响，并且可能减弱这些血管中的α-肾上腺素能收缩。
