中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2010年
4期
376-380
,共5页
李海峰%孙明莉%于亚新%刘晓亮
李海峰%孫明莉%于亞新%劉曉亮
리해봉%손명리%우아신%류효량
心脏骤停%转化生长因子-β1%p38丝裂原活化蛋白激酶%血必净
心髒驟停%轉化生長因子-β1%p38絲裂原活化蛋白激酶%血必淨
심장취정%전화생장인자-β1%p38사렬원활화단백격매%혈필정
Cardiac arrest(CA) transforming growth factor-beta 1%p38 mitogen activated protein kinase%Xuebijing
目的 探讨窒息至心脏骤停大鼠复苏后心脑TCF-β1和p38mAPK的变化及血必净对其影响.方法 采用呼气末夹闭气管窒息法建立大鼠心脏骤停模型,并心肺复苏成功后生存24 h,将50只健康Wistar大鼠随机(随机数字法)分为5组,分别为:模型组,正常埘照组,小剂量血必净组,中剂量血必净组,大剂量血必净组.复苏24 h后处死大鼠,取心、脑组织标本,电镜下观察心、脑组织的病理改变.采用酶联免疫吸附法(EUSA)榆测心、脑组织巾的TCF-β1和p38MAPK含量变化.结果 心、脑组织病理观察显示,与对照组相比其他组心脑细胞超微结构出现损伤性改变,其中模型组损伤最重,大剂量血必净组损伤性改变轻微;心、脑中TGF-β1和p38MAPK含量变化,与对照组相比模型组心、脑TCV-β1和p38MAPK含量升高明显,与模型组相比血必净治疗组心、脑VCF-β1含量升高更明显和P38NAPK含量下降更明显,治疗组中,大剂量较小剂量TCF-β1含量升高更明显和p38NAPK含量下降更为明显.结论 心跳骤停复苏后大鼠心、脑组织内TCF-β1和p38MAPK含量增多,血必净可明显调节心、脑组织中的TCF-β1和p38MAPK含量,而且存在明显量-效关系,从而缓解心跳骤停大鼠复苏中缺氧及再灌注后炎性因子所带来的损伤.
目的 探討窒息至心髒驟停大鼠複囌後心腦TCF-β1和p38mAPK的變化及血必淨對其影響.方法 採用呼氣末夾閉氣管窒息法建立大鼠心髒驟停模型,併心肺複囌成功後生存24 h,將50隻健康Wistar大鼠隨機(隨機數字法)分為5組,分彆為:模型組,正常塒照組,小劑量血必淨組,中劑量血必淨組,大劑量血必淨組.複囌24 h後處死大鼠,取心、腦組織標本,電鏡下觀察心、腦組織的病理改變.採用酶聯免疫吸附法(EUSA)榆測心、腦組織巾的TCF-β1和p38MAPK含量變化.結果 心、腦組織病理觀察顯示,與對照組相比其他組心腦細胞超微結構齣現損傷性改變,其中模型組損傷最重,大劑量血必淨組損傷性改變輕微;心、腦中TGF-β1和p38MAPK含量變化,與對照組相比模型組心、腦TCV-β1和p38MAPK含量升高明顯,與模型組相比血必淨治療組心、腦VCF-β1含量升高更明顯和P38NAPK含量下降更明顯,治療組中,大劑量較小劑量TCF-β1含量升高更明顯和p38NAPK含量下降更為明顯.結論 心跳驟停複囌後大鼠心、腦組織內TCF-β1和p38MAPK含量增多,血必淨可明顯調節心、腦組織中的TCF-β1和p38MAPK含量,而且存在明顯量-效關繫,從而緩解心跳驟停大鼠複囌中缺氧及再灌註後炎性因子所帶來的損傷.
목적 탐토질식지심장취정대서복소후심뇌TCF-β1화p38mAPK적변화급혈필정대기영향.방법 채용호기말협폐기관질식법건립대서심장취정모형,병심폐복소성공후생존24 h,장50지건강Wistar대서수궤(수궤수자법)분위5조,분별위:모형조,정상시조조,소제량혈필정조,중제량혈필정조,대제량혈필정조.복소24 h후처사대서,취심、뇌조직표본,전경하관찰심、뇌조직적병리개변.채용매련면역흡부법(EUSA)유측심、뇌조직건적TCF-β1화p38MAPK함량변화.결과 심、뇌조직병리관찰현시,여대조조상비기타조심뇌세포초미결구출현손상성개변,기중모형조손상최중,대제량혈필정조손상성개변경미;심、뇌중TGF-β1화p38MAPK함량변화,여대조조상비모형조심、뇌TCV-β1화p38MAPK함량승고명현,여모형조상비혈필정치료조심、뇌VCF-β1함량승고경명현화P38NAPK함량하강경명현,치료조중,대제량교소제량TCF-β1함량승고경명현화p38NAPK함량하강경위명현.결론 심도취정복소후대서심、뇌조직내TCF-β1화p38MAPK함량증다,혈필정가명현조절심、뇌조직중적TCF-β1화p38MAPK함량,이차존재명현량-효관계,종이완해심도취정대서복소중결양급재관주후염성인자소대래적손상.
Objective To observe the changes of transforming growth factor-beta 1 (TGF-β1) and p38 mito-gen activated protein kinase (p 38MAPK) , and the effects of Xuebijing on rats during cardiopulmonary cerebral re-suscitation. Method The animal model of cardiac arrest (CA) was made by clamping endotracheal tube at expi-ration, and it survived over 24 hours after cardiopulmonary resuscitation (CPR). Fifty healthy Wistar rats were randomly (random number) divided into control group, model group, small dose of Xuebijing group, medium dose of Xuebijing group and large dose of Xuebijing group. Those rats were sacrificed 24 hours later and the cortex of the brain and the heart were taken out immediately to observe the ultrastructure changes. The levels of TGF-β1 and p38MAPK were determined by using ELISA. Results Compared with control group, the ultrastructure of brain and cardiac tissues were damaged in all other groups, and the most severe damage was seen in the model group, and the leastamage was found in large dose of Xuebijing group. The levels of TGF-β1 in tissues of brain and heart of rats increased more significantly, while the levels of p38MAPK reduced more markedly in Xuebijing treated groups than those did in model group. The magnitudes of increase in TGF-β1 and decrease in p38MAPK were greater in medium dose of Xuebijing group and large dose of Xuebijing group than those in small dose of Xuebijing group. Conclusions The expressions of TGF-β1 and p38MAPK in brain and heart tissues of rats increase after cardiopulmonary cerebral resuscitation. The Xuebijing could significantly modulate the expressions of TGF-β1 and p38MAPK leading to lessening the damage of brain and heart in dose-dependent manner after CPR.
