高压氧对短暂脑缺血大鼠血浆降钙素基因相关肽和β-内啡肽的影响
고압양대단잠뇌결혈대서혈장강개소기인상관태화β-내배태적영향
Effect of hyperbaric oxygen on plasma calcitonin gene-related peptide and beta-enderphin levels in rats with transient global brain ischemia
  • 万方数据
    中国临床康复 중국림상강복
    CHINESE JOURNAL OF CLINICAL REHABILITATION
    2006年 4期 169-171 ,共3页

    陈瑞%付慧芳%谭延国

    진서%부혜방%담연국

    高压氧%脑缺血%再灌注%降钙素基因相关肽%β-内啡肽%疾病模型,动物%脑 高壓氧%腦缺血%再灌註%降鈣素基因相關肽%β-內啡肽%疾病模型,動物%腦
    고압양%뇌결혈%재관주%강개소기인상관태%β-내배태%질병모형,동물%뇌
    背景:缺血早期脑组织损伤是急性脑卒中治疗面临的主要挑战.此期应用高压氧治疗是否对脑组织有明确的保护作用.目的:观察大鼠脑缺血再灌注后,高压氧诱导降钙素基因相关肽和β-内啡肽的动态变化以及高压氧治疗对其的影响,探讨高压氧的治疗作用.设计:随机对照实验.单位:首都医科大学动物科学部.材料:实验于2003-12/2005-02在首都医科大学动物科学部进行.选择清洁级雌性SD大鼠63只按随机数字表分为9组:假手术组7只;缺血再灌注组分别取再灌注6,24,48,96 h时相点组,每组各7只;缺血再灌注+高压氧处理组分别取再灌注6,24,48,96 h时相点组,每组各7只.干预:除假手术组外,其余各组建立脑缺血再灌注动物模型,夹闭双侧颈总动脉缺血20 min后再通血流,假手术组同样手术,但不夹闭颈总动脉.假手术组和缺血再灌注组置于常压空气中,缺血再灌注+高压氧处理组治疗方案为:纯氧洗高压氧舱5 min,升压5 min,然后稳压在0.2 MPa下吸纯氧45 min,缓慢减压15 min,出舱第1天在再灌注3 h后行高压氧处理1次,以后均在3天同一时间作相同处理.缺血再灌注组和缺血再灌注+高压氧处理组分别于再灌注6,24,48,96 h取血.主要观察指标:用放射免疫测定法测定各组血浆中降钙素基因相关肽和β-内啡肽的含量.结果:63只大鼠均进入结果分析.①缺血再灌注6h:高压氧组降钙素基因相关肽应激性升高(64.12±18.16)ng/L,出现时间较缺血再灌注组早,高于同时相点缺血再灌注组(32.62±11.72)ng/L和假手术组(49.09±8.59)ng/L(F=6.614,P＜0.001,P＜0.05);高压氧组β-内啡肽一过性增高.②缺血再灌注24 h和48 h:高压氧处理组降钙素基因相关肽从24 h起即恢复至正常[(43.53±22.73)ng/L,F=0.390;(46.02±10.64)ng/L,F=0.969,P均＞0.05].③缺血再灌注96 h:缺血再灌注组降钙素基因相关肽应激性(81.74±20.64)ng/L,高于假手术组(49.09±8.59)ng/L和同时相点高压氧组(40.98±20.52)ng/L(F=6.419,P＜0.01);并明显高于6,24,48 h的缺血再灌注组组(F=10.806,P均＜0.01).高压氧组β-内啡肽水平降至最低,明显低于假手术组[(370.00±130.15,872.30±403.92)ng/L,(F=3.691,P＜0.05)].结论:①早期高压氧治疗可通过升高血浆降钙素基因相关肽水平和降低β-内啡肽水平以减少梗死区的脑组织损伤.②随高压氧治疗次数的增多,其疗效更好.
    배경:결혈조기뇌조직손상시급성뇌졸중치료면림적주요도전.차기응용고압양치료시부대뇌조직유명학적보호작용.목적:관찰대서뇌결혈재관주후,고압양유도강개소기인상관태화β-내배태적동태변화이급고압양치료대기적영향,탐토고압양적치료작용.설계:수궤대조실험.단위:수도의과대학동물과학부.재료:실험우2003-12/2005-02재수도의과대학동물과학부진행.선택청길급자성SD대서63지안수궤수자표분위9조:가수술조7지;결혈재관주조분별취재관주6,24,48,96 h시상점조,매조각7지;결혈재관주+고압양처리조분별취재관주6,24,48,96 h시상점조,매조각7지.간예:제가수술조외,기여각조건립뇌결혈재관주동물모형,협폐쌍측경총동맥결혈20 min후재통혈류,가수술조동양수술,단불협폐경총동맥.가수술조화결혈재관주조치우상압공기중,결혈재관주+고압양처리조치료방안위:순양세고압양창5 min,승압5 min,연후은압재0.2 MPa하흡순양45 min,완만감압15 min,출창제1천재재관주3 h후행고압양처리1차,이후균재3천동일시간작상동처리.결혈재관주조화결혈재관주+고압양처리조분별우재관주6,24,48,96 h취혈.주요관찰지표:용방사면역측정법측정각조혈장중강개소기인상관태화β-내배태적함량.결과:63지대서균진입결과분석.①결혈재관주6h:고압양조강개소기인상관태응격성승고(64.12±18.16)ng/L,출현시간교결혈재관주조조,고우동시상점결혈재관주조(32.62±11.72)ng/L화가수술조(49.09±8.59)ng/L(F=6.614,P＜0.001,P＜0.05);고압양조β-내배태일과성증고.②결혈재관주24 h화48 h:고압양처리조강개소기인상관태종24 h기즉회복지정상[(43.53±22.73)ng/L,F=0.390;(46.02±10.64)ng/L,F=0.969,P균＞0.05].③결혈재관주96 h:결혈재관주조강개소기인상관태응격성(81.74±20.64)ng/L,고우가수술조(49.09±8.59)ng/L화동시상점고압양조(40.98±20.52)ng/L(F=6.419,P＜0.01);병명현고우6,24,48 h적결혈재관주조조(F=10.806,P균＜0.01).고압양조β-내배태수평강지최저,명현저우가수술조[(370.00±130.15,872.30±403.92)ng/L,(F=3.691,P＜0.05)].결론:①조기고압양치료가통과승고혈장강개소기인상관태수평화강저β-내배태수평이감소경사구적뇌조직손상.②수고압양치료차수적증다,기료효경호.
    BACKGROUND: Prevention of tissue damage during early hours of cerebral ischemia has remained a major challenge in acute stroke management.Whether the application of hyperbaric oxygen (HBO) can protect cerebraltissue or not remains a question to be answered.OBJECTIVE: In cerebral ischemia-reperfusion rat model we studied the change on CGRP and β-endorphine levels and the therapeutic implication with hyperbaric oxygenation.DESIGN: A randomized controlled animal study.SETTING: Animal Research Department of Capital University of Medical Science.MATERIALS: The experiment was carried out at the Animal Research Department of the Capital University of Medical Science from December 2003 to February 2005. Sixty three healthy Sprague-Dewey female rats were randomly divided into 9 groups. There were 7 in the sham operation group. Four groups with 7 in each group received cerebral ischemia followed by reperfusion (IR) and blood sample taken at 6, 24, 48 and 96 hourrespectively. Another 4 groups (IR-HBO) with 7 in each received cerebral ischemia and reperfusion under hyperbaric oxgenation with blood sampling at 6, 24, 48 and 96 hours.INTERVENTIONS: With the exception of sham operation groups, animals in all the experimental groups were exposed to global cerebral is chemia of 20 minutes duration. Sham operation group and the IR groups remained under the normal atmospheric pressure. The HBO chamber was flushed with 100% oxygen for 5 minutes and raised the pressure in 5 minutes to a steady pressure at 0.2MPa. Rats in IR-HBO groups were put into the chamber with inhalation of 100% oxygen for 45 minutes and decompression was done for 15 minutes. The rats in HBO group were placed into the HBO chamber after 3-hour post reperfusion on the first day and this treatment was repeated for three consecutive days, always at the same time.Plasma was collected after 6 hours, 24 hours, 48 hours or 96 hours post cerebral reperfusion, respectively.MAIN OUTCOME MEASURES: The level of CGRP and β-EP in the plasma were measured by RIA (Radio-immunoassay).RESULTS: Sixty-three rats entered the final analysis. ① At 6-hour ischemia-repefusion: CGRP in HBO group was increased (64.12±18.16) ng/L and the onset time was earlier than that in IR group and the level was higher than those in IR group (32.62 ±11.72)ng/L and sham operation group (49.09±8.59)ng/L at the same time point (F=6.614, P ＜ 0.001, P ＜ 0.05). Β-EP level in 6-hour HBO group was slightly increased, but recovered at 24-hour, 48-hour, 96-hour HBO groups. ② At 24-hour and 48-hour ischemia-reperfusion: The plasma CGRP levels of the HBO group recover within 24-hours [(43.53±22.73)ng/L, F=0.390; (46.02±10.64)ng/L,F=0.969, P ＞ 0.05]. ③ 96-hour ischemia-reperfusion: CGRP increase in the IR group (81.74±20.64)ng/L was higher than that in the sham operation group (49.09±8.59)ng/L and the HBO group (40.98±20.52)ng/L at the same time point (F=6.419, P ＜ 0.01); and also obviously higher than those in 6-hour, 24-hour and 48-hour IR group (F=10.806, P ＜ 0.01).The β-EP level at 96-hour HBO group was decreased to the lowest as compared with that in the sham operation group [(370.00±130.15)ng/L,(872.30±403.92)ng/L, F=3.691, P ＜ 0.05].CONCLUSION: ① HBO in the early period of cerebral ischemia can reduce the onset of injury of cerebral tissue through increasing CGRP level and decreasing β-EP level; ②The more times treated by HBO, the better is its therapeutic effect.
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