CAJ | 학술논문

目的：建立偏头痛大鼠皮层扩布性抑制（cortical spreading depression, CSD）模型，研究盐酸氟桂利嗪干预后对CSD及血浆降钙素基因相关肽（calcitonin-gene related peptide, CGRP）、P物质（substance P, SP）浓度的影响。方法大鼠随机分为对照组、CSD组、氟桂利嗪干预组，利用氯化钾溶液刺激法建立CSD模型，采用放射免疫技术测定大鼠血浆中的CGRP、SP浓度。结果对照组未记录到CSD波；氟桂利嗪干预组与CSD组比较， CSD波的潜伏期延长[氟桂利嗪干预组(167.90±25.18s) vs.CSD组(130.90±13.30s)](P<0.01)，个数减少[氟桂利嗪干预组(4.50±1.84) vs.CSD组(8.50±2.07)](P<0.01)，波幅降低[氟桂利嗪干预组(11.40±4.12 mv) vs.CSD组(24.40±3.57 mv)](P<0.01)；关于血浆CGRP浓度和SP浓度，CSD组(CGRP,32.95±11.61 pg/mL；SP,27.80±7.51 pg/mL)及氟桂利嗪干预组(CGRP,25.13±5.67 pg/mL；SP,19.45±6.10 pg/mL)均高于对照组(CGRP,14.44±6.39 pg/mL；SP,12.36±4.22 pg/mL)(P<0.01)，氟桂利嗪干预组(CGRP,25.13±5.67 pg/mL；SP,19.45±6.10 pg/mL)低于CSD组(CGRP,32.95±11.61 pg/mL；SP,27.80±7.51 pg/mL)(P<0.05)。结论盐酸氟桂利嗪能够抑制CSD的发生，使大鼠CSD模型的血浆CGRP、SP浓度降低。
목적：건립편두통대서피층확포성억제（cortical spreading depression, CSD）모형，연구염산불계리진간예후대CSD급혈장강개소기인상관태（calcitonin-gene related peptide, CGRP）、P물질（substance P, SP）농도적영향。방법대서수궤분위대조조、CSD조、불계리진간예조，이용록화갑용액자격법건립CSD모형，채용방사면역기술측정대서혈장중적CGRP、SP농도。결과대조조미기록도CSD파；불계리진간예조여CSD조비교， CSD파적잠복기연장[불계리진간예조(167.90±25.18s) vs.CSD조(130.90±13.30s)](P<0.01)，개수감소[불계리진간예조(4.50±1.84) vs.CSD조(8.50±2.07)](P<0.01)，파폭강저[불계리진간예조(11.40±4.12 mv) vs.CSD조(24.40±3.57 mv)](P<0.01)；관우혈장CGRP농도화SP농도，CSD조(CGRP,32.95±11.61 pg/mL；SP,27.80±7.51 pg/mL)급불계리진간예조(CGRP,25.13±5.67 pg/mL；SP,19.45±6.10 pg/mL)균고우대조조(CGRP,14.44±6.39 pg/mL；SP,12.36±4.22 pg/mL)(P<0.01)，불계리진간예조(CGRP,25.13±5.67 pg/mL；SP,19.45±6.10 pg/mL)저우CSD조(CGRP,32.95±11.61 pg/mL；SP,27.80±7.51 pg/mL)(P<0.05)。결론염산불계리진능구억제CSD적발생，사대서CSD모형적혈장CGRP、SP농도강저。
Objective To explore the effects of flunarizine hydrochloride on plasma calcitonin gene-related pep-tide and substance P levels after CSD in a rat migraine model of cortical spreading depression (CSD). Methods Thirty adult rats were randomly and evenly divided into three groups:control Group, CSD group and flunarizine group. The CSD waves were evoked by application of potassium chloride on brain surface with filter paper. Funarizine hydrochloride was intravenously administered to rats five minutes prior to application of potassium chloride. The plasma levels of CGRP and SP were measured by using radioimmunity assay. Statistical analyses were performed using two-sample t test and analy-sis of variance. Results CSD waves were absent in control group whereas CSD waves were induced in CSD and flunari-zine groups. The latency of the first CSD wave was longer in flunarizine group (167.90 ± 25.18 s) than in CSD group (130.90 ± 13.30 s) (P<0.01). The number of CSD waves was smaller in flunarizine group (4.50 ± 1.84) than in CSD group (8.50 ± 2.07) (P<0.01). The amplitude of CSD waves was lower in flunarizine group (11.40 ± 4.12 mv) than in CSD group (24.40±3.57 mv) (P<0.01). The levels of CGRP and SP in both CSD group (CGRP, 32.95±11.61 pg/mL;SP, 27.80±7.51 pg/mL) and flunarizine group (CGRP, 25.13 ± 5.67 pg/mL; SP, 19.45 ± 6.10 pg/mL) were higher than in control group (CGRP, 14.44 ± 6.39 pg/mL; SP, 12.36 ± 4.22 pg/mL) (P<0.01). The levels of CGRP and SP in flunarizine group (CGRP, 25.13±5.67 pg/mL;SP, 19.45±6.10 pg/mL) were lower than those in CSD group (CGRP, 32.95±11.61 pg/mL;SP, 27.80± 7.51 pg/mL) (P<0.05). Conclusions Flunarizine hydrochloride can inhibit CSD and reduce the plama levels of CGRP and SP in the rat model of CSD.