摘要
目的:探讨辣椒素受体-1(TRPV1)、一氧化氮(NO)和降钙素基因相关肽(CGRP)在上颈段脊髓刺激(cSCS)诱导脑血流(CBF)增加中的作用和相互关系。方法:将雄性SD大鼠在全麻下行C1-2椎板切除暴露颈段脊髓,刺激电极放置在左侧C2脊髓背柱上。切开颅骨暴露左侧大脑皮质,CBF变化由激光多普勒血流仪测量。分析90%运动阈值(MT)cSCS在静脉注射辣椒素类似物树胶脂毒素(RTX)2μg/kg(n=9)、CGRP8-37(CGRP受体拮抗剂)2.5mg/kg(n=8)、L-NAME(一氧化氮合酶抑制剂)5.0mg/kg(n=7)前和20min后同侧脑血流变化(%△CBF)及脑血管阻力变化(%△CVR)。结果:60%和90%MT的cSCS使同侧大脑皮质血流增加(P<0.05,n=9)。静脉注射含有TRPV1纤维脱敏化的RTX(2μg/kg)后,90%MT的cSCS引起%△CBF由65.0%±9.5%减少到27.4%±7.2%(P<0.05,n=9),%△CVR由-28%±7.6%增加到-14.8%±4.2%(P<0.05,n=9);静脉注射CGRP8-37(2.5mg/kg)使90%MT的cSCS引起增加的CBF降低(%△CBF:63.4%±10.4%vs.22.7%±5.3%,P<0.05,n=8;%△CVR:-27.9%±5.9%vs.-14.8%±3.2%,P<0.05,n=8);静脉注射L-NAME(5.0mg/kg)使90%MT的cSCS引起增加的CBF显著下降(%△CBF:58.1%±9.5%vs.14.0%±2.5%,P<0.01,n=7;%△CVR:-20.4%±4.3%vs.-7.6%±0.6%,P<0.01,n=7)。结论:TRPV1、NO和CGRP参与cSCS引起显著的脑血流增加或脑血管扩张,它可能为cSCS治疗缺血性脑血管病提供新的理论依据。
Objective：To explore the role and relationship of transient receptor potential vanilloid type 1（TRPV1）,nitric oxide（NO） and calcitonin gene-related peptide（CGRP） in augmentation of cerebral blood flow（CBF） by cervical spinal cord stimulation（cSCS）.Method：Laminectomy was performed to expose the dorsal surface of C1-C2 spinal cord under general anesthetized male rats.The stimulus electrode was placed on the left dorsal column at cervical spinal cord（C2）.Parietal craniotomy was performed to expose the left cortex for placement of laser Doppler flowmetry（LDF） probe to measure CBF.Effects of cSCS at 90% of motor threshold（MT） on ipsilateral CBF and cerebral vascular resistance（CVR） were compared before and 20min after intravenous resiniferatoxin（RTX）（2μg/kg,n=9）,CGRP8-37（2.5mg/kg,n=8）、L-NAME（5.0mg/kg,n=7）.Result：The cSCS at 60% and 90% of MT applied to the dorsal column of upper cervical（C1-C2） ipsilateral spinal segments produced vasodilation in ipsilateral cerebral cortex（P0.05,n=9）.Further,only cSCS at 90% of MT was employed in following procedures.After desensitization of TRPV1-containing neural fibers with intravenous RTX（2μg/kg）,cSCS-induced augmentation of CBF decreased from 65.0±9.5% to 27.4±7.2%（P0.05,n=9）.Accordingly,cerebral vascular resistance（%△CVR） increased from-28.0 ±7.6% to-14.8 ±4.2%（P0.05,n=9）.Intravenous CGRP8-37（2.5mg/kg,n=8） significantly decreased cSCS-induced %△CBF（63.4±10.4% vs.22.7±5.3%,P0.05） and increased %△CVR（-27.9±5.9% vs.-14.8±3.2%,P0.05）.Intravenous L-NAME（5.0mg/kg,n=7）decreased cSCSinduced %△CBF from 58.1±9.5% to 14.0±2.5%（P0.01） and increased %△CVR from-20.4±4.3% to-7.6±0.6%（P0.01）.Conclusion：TRPV1,NO and CGRP were involved in cSCS-induced augmentation of cerebral blood flow or cerebrovasodilatation.It might provide new theories and evidences for cSCS treatment of ischemic cerebral vascular diseases.
出处
《中国康复医学杂志》
CAS
CSCD
北大核心
2010年第6期491-496,共6页
Chinese Journal of Rehabilitation Medicine
基金
陕西省科技攻关项目(2008K16-06)
美国NIH科研基金(HL075524)
关键词
脊髓刺激
辣椒素受体-1
一氧化氮
降钙素基因相关肽
血管扩张
spinal cord stimulation
transient receptor potential vanilloid type 1
nitric oxide
calcitonin gene-related peptide
vasodilation.
