中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
11期
1384-1387
,共4页
吴会生%郭培培%张宗泽%刘丹彦
吳會生%郭培培%張宗澤%劉丹彥
오회생%곽배배%장종택%류단언
氟比洛芬%再灌注损伤%脑%血脑屏障
氟比洛芬%再灌註損傷%腦%血腦屏障
불비락분%재관주손상%뇌%혈뇌병장
Flurbiprofen%Reperfusion injury%Brain%Blood-brain barrier
目的 探讨氟比洛芬酯预先给药对全脑缺血再灌注大鼠血脑屏障通透性的影响.方法 健康雄性SD大鼠45只,体重300~350 g,随机分为3组(n=15):假手术组(S组)、缺血再灌注组(IR组)和氟比洛芬酯预先给药组(F组).采用夹闭双侧颈总动脉联合低血压法建立全脑缺血再灌注模型.S组仅分离双侧颈总动脉,不结扎;IR组、F组于脑缺血前15 min经右颈总静脉分别注射氟比洛芬酯空白乳剂1 ml/kg(容量与F组一致)、氟比洛芬酯10 mg/kg.再灌注24 h时,静脉注射伊文思蓝(EB)3 ml/kg.取脑组织,观察病理学结果,测定神经元凋亡率、脑含水量、脑组织EB、TNF-α、IL-1β及IL-10的含量.结果 与S组比较,IR组和F组神经元凋亡率、脑含水量、脑组织EB、TNF-α、IL-1β及IL-10含量升高(P<0.05或0.01);与IR组比较,F组神经元凋亡率、脑含水量和脑组织EB、TNF-α和IL-1β的含量降低,IL-10含量升高(P<0.05或0.01).F组脑组织病理学损伤较IR组减轻.结论 氟比洛芬酯预先给药可降低全脑缺血再灌注大鼠血脑屏障通透性,减轻脑损伤,其机制可能与抑制炎性反应有关.
目的 探討氟比洛芬酯預先給藥對全腦缺血再灌註大鼠血腦屏障通透性的影響.方法 健康雄性SD大鼠45隻,體重300~350 g,隨機分為3組(n=15):假手術組(S組)、缺血再灌註組(IR組)和氟比洛芬酯預先給藥組(F組).採用夾閉雙側頸總動脈聯閤低血壓法建立全腦缺血再灌註模型.S組僅分離雙側頸總動脈,不結扎;IR組、F組于腦缺血前15 min經右頸總靜脈分彆註射氟比洛芬酯空白乳劑1 ml/kg(容量與F組一緻)、氟比洛芬酯10 mg/kg.再灌註24 h時,靜脈註射伊文思藍(EB)3 ml/kg.取腦組織,觀察病理學結果,測定神經元凋亡率、腦含水量、腦組織EB、TNF-α、IL-1β及IL-10的含量.結果 與S組比較,IR組和F組神經元凋亡率、腦含水量、腦組織EB、TNF-α、IL-1β及IL-10含量升高(P<0.05或0.01);與IR組比較,F組神經元凋亡率、腦含水量和腦組織EB、TNF-α和IL-1β的含量降低,IL-10含量升高(P<0.05或0.01).F組腦組織病理學損傷較IR組減輕.結論 氟比洛芬酯預先給藥可降低全腦缺血再灌註大鼠血腦屏障通透性,減輕腦損傷,其機製可能與抑製炎性反應有關.
목적 탐토불비락분지예선급약대전뇌결혈재관주대서혈뇌병장통투성적영향.방법 건강웅성SD대서45지,체중300~350 g,수궤분위3조(n=15):가수술조(S조)、결혈재관주조(IR조)화불비락분지예선급약조(F조).채용협폐쌍측경총동맥연합저혈압법건립전뇌결혈재관주모형.S조부분리쌍측경총동맥,불결찰;IR조、F조우뇌결혈전15 min경우경총정맥분별주사불비락분지공백유제1 ml/kg(용량여F조일치)、불비락분지10 mg/kg.재관주24 h시,정맥주사이문사람(EB)3 ml/kg.취뇌조직,관찰병이학결과,측정신경원조망솔、뇌함수량、뇌조직EB、TNF-α、IL-1β급IL-10적함량.결과 여S조비교,IR조화F조신경원조망솔、뇌함수량、뇌조직EB、TNF-α、IL-1β급IL-10함량승고(P<0.05혹0.01);여IR조비교,F조신경원조망솔、뇌함수량화뇌조직EB、TNF-α화IL-1β적함량강저,IL-10함량승고(P<0.05혹0.01).F조뇌조직병이학손상교IR조감경.결론 불비락분지예선급약가강저전뇌결혈재관주대서혈뇌병장통투성,감경뇌손상,기궤제가능여억제염성반응유관.
Objective To investigate the effects of flurbiprofen pretreatment on the permeability of bloodbrain barrier in a rat model of global cerbral ischemia-reperfusion (I/R) injury. Methods Forty-five male SD rats weighing 300-350 g were randomly divided into 3 groups (n = 15 each): sham operation group (group S); global cerebral I/R group (group I/R); flurbiprofen 10 mg/kg + global cerebral I/R group (group F). Global cerebral ischemia was induced by 20 min occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg). In group F, flurbiprofen 10 mg/kg was injected iv at 15 min before ischemia. Evans blue 3 ml/kg was injectcd iv at 24 h of reperfusion, then the rats were sacrificed and their brains were immediately removed for determination of the apoptosis rate, brain water content, Evans blue content, TNF-α, IL-1β and IL-10 content, and microscopic examination. Results The apoptosis rate, brain water content, Evans blue content, and TNF-α, IL-1β and IL-10 content were significantly higher in group I/R and F than in group S (P < 0.05 or 0.01).The apoptosis rate, brain water content, and Evans blue content and TNF-α and IL-1β content were significantly lower, while IL-10 content was higher in group F than in group I/R (P < 0.01). Global cerbral I/R-induced changes were significantly attenuated in group F. Conclusion Pretreatment with flurbiprofen can protect bloodbrain barrier against cerebral I/R injury by inhibition of the inflammatory reaction.