摘要
目的探讨交感神经系统中的一氧化氮合酶(NOS)对血管平滑肌增殖的影响及调控。方法用三氯化铁(FeCl3)损伤颈总动脉建立大鼠平滑肌增殖模型,实验分为假手术组、术后存活1d组、5d组,在5d组中加设注射抑制剂N-硝基-L精氨酸(LNNA)组,每组6只大鼠,采用还原型尼克酰胺腺嘌呤二核苷酸黄递酶(NADPH-d)组织化学染色和荧光金(FG)逆向追踪双标,观察颈交感神经节和脊髓中间外侧核神经细胞一氧化氮合酶的变化;苏木素-伊红(HE)染色观察血管平滑肌增殖变化。结果血管损伤后1d、5d组的颈交感神经节中有较多NADPH-d染色阳性细胞表达,尤其5d组更明显;手术侧的T1~T3脊髓侧角NADPH-d阳性细胞数也增多,而抑制剂组的NADPH-d阳性细胞数明显减少;HE染色可见血管损伤后有平滑肌增殖,而抑制剂组增殖更明显。结论损伤颈总动脉后颈交感神经节和T1~T3脊髓侧角内的NOS活性增强,可能参与血管平滑肌细胞(VSMC)增殖的调控。
Objective To investigate the influence of the nitric oxide synthase(NOS) in the sympathetic nervous system on proliferation of vascular smooth muscle. Methods The model of proliferation of vascular smooth muscle was established by injuring common carotid artery by FeCl3. Twenty-four SD rats were divided into 4 experimental groups: sham operation group, survival 1 day group, survival 5 days group and N-nitro-L-arginine (LNNA) treatment group. Cervical sympathetic ganglion and spinal cord intermediolateral nucleus were retrogradely labeled by injection of 3% fluorogold(FG) into carotid sheath and cervical sympathetic ganglion, and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) reactivity was detected histoehemieally. The proliferation of vascular smooth muscle was observed by hematoxylin-eosin(HE) staining. Results Compared to sham operation group, NADPH-positive neurons of cervical sympathetic ganglion and spinal cord intermediolateral nucleus were increased in survival 1 day and 5 days group,especially 5 days group, but decreased in LNNA group. The proliferation of vascular smooth muscle was significantly increased in LNNA group as indicated by HE staining. Conclusion The NOS of the sympathetic nervous system plays an important role on proliferation of vascular smooth muscle after injuring common carotid artery.
出处
《解剖学报》
CAS
CSCD
北大核心
2010年第5期670-673,共4页
Acta Anatomica Sinica
基金
苏州大学创新团队项目资助(9034602)
苏州大学医学发展基金资助项目(EE134519)