摘要
目的通过观察一氧化氮(NO)对延迟皮瓣微循环的影响来探讨皮瓣血管舒张的机制。方法采用CD-1白鼠为实验动物,在其背部形成1.0cm×3.0cm延迟皮瓣。通过体内视频显微法和激光多普勒血流仪,分别检测皮瓣血管直径和血流量,观察一氧化氮合成前体L-精氨酸(L-arg)对皮瓣微循环的影响。结果在延迟皮瓣前,血管的平均直径范围为(22.15±3.65)μm~(25.32±3.34)μm,平均血流量为(1.84±0.74)nl/s~(2.31±0.91)nl/s;延迟皮瓣后,对照组血管直径增加到(43.83±11.17)μm,血流量增加到(6.98±3.12)nl/s。三天后,随着L-Arg剂量的增加,治疗组与对照组相比,血管直径大小和血流量显著增加(P<0.05)。结论一氧化氮在延迟皮瓣微循环中发挥了重要作用,它主要通过扩张血管和增加血流量来实现的。
Objective To elucidate the mechanism of vasodilation by exploring the effects of nitric oxide on the microcirculation of skin flap delay. Methods Using a skin flap model in CD-1 white mice, a skin flap delay( 1.0cm × 3.0cm) was designed on the back of a white mouse. The diameter of artery was measured by using in vivo videomicroscopy, vessel flow was measured by using an optical Doppler velocimeter, observe the effects of NO synthase substrate(L-arginine) on the microcirculation of skin flap delay. Results Average vessel diameter ranged from( 22. 15 ± 3.65)μm to( 25.32 ± 3.34)μm before skin flap delay, average flow ranged from( 1.84 ± 0.74) nl/sec to( 2.31 ±0.91) nl/sec before delay; vessel diameter increased to(43.83 ± 11.17)μm and vessel flow increased to(6.98 ±3.12)nl/sec in the control animals after delay. As the dose of L-arg increased in treated animals, there was significant increase in vessel diameter and flow after three days. Conclusion Nitric oxide is an important element of vasodilation and contributor to the phenomenon of skin flap delay.
出处
《中国微循环》
北大核心
2008年第1期8-10,共3页
Journal of Chinese Microcirculation
基金
浙江省教育厅资助项目(20061835)