Li Z, Koman L A, Rosencrance E, Smith B P, Smith T L
Department of Orthopaedic Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.
J Cardiovasc Pharmacol. 1998 Sep;32(3):349-56. doi: 10.1097/00005344-199809000-00003.
The role of nitric oxide (NO) in the control of arteriovenous anastomoses (AVAs) has not been studied in vivo in a thermoregulatory end organ. In this study, the effect of local inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME) on the microvasculature in the rabbit ear (n=12) was observed in vivo through a chronically implanted ear microvascular chamber. Ear cutaneous blood perfusion (CBP), total auricular arterial flow (TAF), and ear temperature were monitored simultaneously with the direct microvascular observations. Results revealed that intrafacial artery infusion of L-NAME produced significant vasoconstriction of arterioles, AVAs, and venules (p < 0.05). A decrease of ear blood perfusion also was demonstrated by changes of CBP, TAF, and surface temperature. The data provide evidence that basal generation of NO influences the vascular resistance in the thermoregulatory end organ. Moreover, endogenous NO production may be more important in regulating the AVA flow than is flow in other parts of the rabbit ear microvasculature. The effects of NO inhibition on ear microvasculature were not abolished by superior cervical ganglionectomy, indicating that NO production in the rabbit ear is not a neurally mediated mechanism. Further study with a short-term rabbit ear preparation showed that inhibition of NO production with L-NAME enhanced microvascular constrictive responses to extraluminal application of norepinephrine. NO thus appears to play a role of basal vasodilator in opposition to the basal adrenergic vasoconstrictor tone in the rabbit ear.
一氧化氮（NO）在体温调节终末器官中对动静脉吻合支（AVA）的控制作用尚未在体内进行研究。在本研究中，通过长期植入的耳部微血管腔在体内观察了NG-硝基-L-精氨酸甲酯（L-NAME）局部抑制NO合成对兔耳（n = 12）微血管系统的影响。在进行微血管直接观察的同时，同步监测耳部皮肤血液灌注（CBP）、耳总动脉血流量（TAF）和耳温。结果显示，向面动脉内注入L-NAME可使小动脉、AVA和小静脉产生显著的血管收缩（p < 0.05）。CBP、TAF和表面温度的变化也证实了耳部血液灌注的减少。这些数据提供了证据，表明NO的基础生成会影响体温调节终末器官中的血管阻力。此外，内源性NO生成在调节AVA血流方面可能比在兔耳微血管系统的其他部位的血流调节中更为重要。上颈神经节切除并未消除NO抑制对兔耳微血管系统的影响，这表明兔耳中NO的产生不是一种神经介导机制。对短期兔耳标本的进一步研究表明，用L-NAME抑制NO生成可增强微血管对管腔外应用去甲肾上腺素的收缩反应。因此，NO似乎在兔耳中作为基础血管舒张剂发挥作用，对抗基础肾上腺素能血管收缩张力。
