背景:高压氧可增加氧弥散能力,从而改善脑水肿和脑组织缺氧,促进病灶区脑细胞的生理功能恢复、侧支循环的建立和脑细胞再生修复.目的:观察高压氧对大鼠急性局灶性脑缺血再灌注损伤后不同时间点c-fos癌基因表达的影响.设计:随机分组动物实验.单位:解放军第四军医大学唐都医院急诊科、西安高新医院检验中心、解放军空军总医院、解放军第四军医大学航空航天医学系高压氧治疗中心.材料:实验于2002-04在解放军第四军医大学航空航天医学系高压氧治疗中心完成,选用65只生后2个月健康雄性SD大鼠.方法:随机摸球法将大鼠分为4组,模型组(n=20):参照Koizumi等设计的方法,制备大鼠大脑中动脉缺血模型;正常对照组(n=5):手术方式同模型组,但不阻断动脉血流;纯氧治疗组(n=20):手术过程同模型组,动物缺血1 h后抽出栓子,分别在插入栓子后2,9,21,45,69 h将动物置于高压舱内,常压下吸100%纯氧.高压氧治疗组(n=20):手术过程同模型组,动物缺血1 h后抽出栓子,分别在插入栓子后2,9,21,45,69 h将动物置于高压氧舱内,0.25 MPa吸纯氧1 h.主要观察指标:利用免疫组织化学和病理组织学法观察各组大鼠脑缺血再灌注5,12,24,72 h脑皮质、视前区与纹状体中性白细胞浸润及c-fos癌基因蛋白及阳性细胞表达的变化;计算脑缺血再灌注72 h皮质、纹状体内侧区与视前区神经元坏死程度、大鼠左侧半球脑血管渗漏面积.结果:纳入大鼠65只均进入结果分析.①视前区c-fos阳性产物主要集中于中部.对侧皮质少见c-fos阳性反应,视前区有轻度表达,纹状体呈中等强度的反应.缺血12 h,c-fos阳性产物在上述区域开始减弱,24 h强度明显减弱;高压氧治疗组皮质和视前区较单纯缺血组c-fos阳性产物强度明显减弱;缺血再灌注12 h,高压氧治疗组视前区、纹状体中性白细胞数明显低于模型组(P＜0.05);缺血再灌注24 h,脑皮质、视前区、纹状体中性白细胞低于模型组(P＜0.05).②高压氧治疗组血管渗漏面积与单纯模型组相比明显缩小(P＜0.05);缺血再灌注72 h,高压氧治疗组视交叉平面皮质、纹状体内侧区与视前区神经细胞损伤数目较模型组明显减轻(P＜0.05),假手术组未见神经元损伤.结论:高压氧可明显缩小大鼠急性局灶性脑缺血再灌注损伤的血管渗漏面积,减轻神经系统症状,抑制中性白细胞浸润,抑制梗塞区c-fos癌基因表达,减少"半影区"神经元坏死.
揹景:高壓氧可增加氧瀰散能力,從而改善腦水腫和腦組織缺氧,促進病竈區腦細胞的生理功能恢複、側支循環的建立和腦細胞再生脩複.目的:觀察高壓氧對大鼠急性跼竈性腦缺血再灌註損傷後不同時間點c-fos癌基因錶達的影響.設計:隨機分組動物實驗.單位:解放軍第四軍醫大學唐都醫院急診科、西安高新醫院檢驗中心、解放軍空軍總醫院、解放軍第四軍醫大學航空航天醫學繫高壓氧治療中心.材料:實驗于2002-04在解放軍第四軍醫大學航空航天醫學繫高壓氧治療中心完成,選用65隻生後2箇月健康雄性SD大鼠.方法:隨機摸毬法將大鼠分為4組,模型組(n=20):參照Koizumi等設計的方法,製備大鼠大腦中動脈缺血模型;正常對照組(n=5):手術方式同模型組,但不阻斷動脈血流;純氧治療組(n=20):手術過程同模型組,動物缺血1 h後抽齣栓子,分彆在插入栓子後2,9,21,45,69 h將動物置于高壓艙內,常壓下吸100%純氧.高壓氧治療組(n=20):手術過程同模型組,動物缺血1 h後抽齣栓子,分彆在插入栓子後2,9,21,45,69 h將動物置于高壓氧艙內,0.25 MPa吸純氧1 h.主要觀察指標:利用免疫組織化學和病理組織學法觀察各組大鼠腦缺血再灌註5,12,24,72 h腦皮質、視前區與紋狀體中性白細胞浸潤及c-fos癌基因蛋白及暘性細胞錶達的變化;計算腦缺血再灌註72 h皮質、紋狀體內側區與視前區神經元壞死程度、大鼠左側半毬腦血管滲漏麵積.結果:納入大鼠65隻均進入結果分析.①視前區c-fos暘性產物主要集中于中部.對側皮質少見c-fos暘性反應,視前區有輕度錶達,紋狀體呈中等彊度的反應.缺血12 h,c-fos暘性產物在上述區域開始減弱,24 h彊度明顯減弱;高壓氧治療組皮質和視前區較單純缺血組c-fos暘性產物彊度明顯減弱;缺血再灌註12 h,高壓氧治療組視前區、紋狀體中性白細胞數明顯低于模型組(P＜0.05);缺血再灌註24 h,腦皮質、視前區、紋狀體中性白細胞低于模型組(P＜0.05).②高壓氧治療組血管滲漏麵積與單純模型組相比明顯縮小(P＜0.05);缺血再灌註72 h,高壓氧治療組視交扠平麵皮質、紋狀體內側區與視前區神經細胞損傷數目較模型組明顯減輕(P＜0.05),假手術組未見神經元損傷.結論:高壓氧可明顯縮小大鼠急性跼竈性腦缺血再灌註損傷的血管滲漏麵積,減輕神經繫統癥狀,抑製中性白細胞浸潤,抑製梗塞區c-fos癌基因錶達,減少"半影區"神經元壞死.
배경:고압양가증가양미산능력,종이개선뇌수종화뇌조직결양,촉진병조구뇌세포적생리공능회복、측지순배적건립화뇌세포재생수복.목적:관찰고압양대대서급성국조성뇌결혈재관주손상후불동시간점c-fos암기인표체적영향.설계:수궤분조동물실험.단위:해방군제사군의대학당도의원급진과、서안고신의원검험중심、해방군공군총의원、해방군제사군의대학항공항천의학계고압양치료중심.재료:실험우2002-04재해방군제사군의대학항공항천의학계고압양치료중심완성,선용65지생후2개월건강웅성SD대서.방법:수궤모구법장대서분위4조,모형조(n=20):삼조Koizumi등설계적방법,제비대서대뇌중동맥결혈모형;정상대조조(n=5):수술방식동모형조,단불조단동맥혈류;순양치료조(n=20):수술과정동모형조,동물결혈1 h후추출전자,분별재삽입전자후2,9,21,45,69 h장동물치우고압창내,상압하흡100%순양.고압양치료조(n=20):수술과정동모형조,동물결혈1 h후추출전자,분별재삽입전자후2,9,21,45,69 h장동물치우고압양창내,0.25 MPa흡순양1 h.주요관찰지표:이용면역조직화학화병리조직학법관찰각조대서뇌결혈재관주5,12,24,72 h뇌피질、시전구여문상체중성백세포침윤급c-fos암기인단백급양성세포표체적변화;계산뇌결혈재관주72 h피질、문상체내측구여시전구신경원배사정도、대서좌측반구뇌혈관삼루면적.결과:납입대서65지균진입결과분석.①시전구c-fos양성산물주요집중우중부.대측피질소견c-fos양성반응,시전구유경도표체,문상체정중등강도적반응.결혈12 h,c-fos양성산물재상술구역개시감약,24 h강도명현감약;고압양치료조피질화시전구교단순결혈조c-fos양성산물강도명현감약;결혈재관주12 h,고압양치료조시전구、문상체중성백세포수명현저우모형조(P＜0.05);결혈재관주24 h,뇌피질、시전구、문상체중성백세포저우모형조(P＜0.05).②고압양치료조혈관삼루면적여단순모형조상비명현축소(P＜0.05);결혈재관주72 h,고압양치료조시교차평면피질、문상체내측구여시전구신경세포손상수목교모형조명현감경(P＜0.05),가수술조미견신경원손상.결론:고압양가명현축소대서급성국조성뇌결혈재관주손상적혈관삼루면적,감경신경계통증상,억제중성백세포침윤,억제경새구c-fos암기인표체,감소"반영구"신경원배사.
BACKGROUND:Hyperbaric oxygen (HBO) can increase oxygen diffusing capacity, thereby, improve hypoxic state of brain edema and brain tissue and promote the recovery of physiological function of brain cells in focal zone, the establishment of bypass circuit, and regeneration and repair of brain cells.OBJECTIVE: To observe the effect of hyperbaric oxygen on c-fos oncogene expression of rats at different time points following acute focal cerebral ischemia/reperfusion(I/R) injury.DESIGN : Randomized grouping animal experiment.SETTING: Department of Emergency, Tangdu Hospital, Fourth Military Medical University of Chinese PLA; Department of Laboratory Medicine, Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA; Hyperbaric Oxygen Treatment Center, Department of Aerospace Medicine, Fourth Military Medical University of Chinese PLA.MATERIALS: This experiment was carried out in the Hyperbaric Oxygen Treatment Center, Department of Aerospace Medicine, Fourth Military Medical University of Chinese PLA in April 2002. Sixty-five 2-month-old healthy male SD rats.METHODS: The involved rats were randomized into: model group (n =20), normal control group (n =5), pure oxygen treatment group (n =20) and HBO treatment group (n =20). In the model group, following the method of Koizumi et al, rat models of middle cerebral artery (MCA) ischemia were developed. In the normal control group, only occlusion of arterial blood flow was omitted; In the pure oxygen treatment group, the operation procedure was the same as that of model group, and embolus being drawn out at ischemia for 1 hour, rats were placed in the hyperbaric cabin at 2,9,21, 45 and 69 hours after embolus being inserted, and they inhaled pure oxygen under the normal pressure; In the HBO treatment group, the operation procedure was the same as that of model group, and rats inhaled pure oxygen for 1 hour under 0.25 MPa pressure. MAIN OUTCOME MEASURES: By means of immunohistochemical and pathohistological methods, neutrophilic infiltration,c-fos oncogene protein and positive cell expression in cerebral cortex, preoptic area and corpora striatum of rats in each group were observed at cerebral I/R 5, 12, 24 and 72 hours; Neuronal necrosis degree in cerebral cortex, medial area of corpora striatum and preoptic area, and cerebrovascular leakage area of left cerebral hemisphere of rats were calculated.RESULTS: Sixty-five rats were involved in the final analysis. ① c-fos positive products mainly focused in the center of the preoptic area, but they were occasionally seen in the contralateral cortex, slightly expressed in the preoptic area and moderately expressed in the corpora striatum, c-fos positive products began to reduce in the above-mentioned area at ischemia 12 hours, and were obviously reduced at ischemia 24 hours; c-fos positive products in the cerebral cortex and preoptic area were obviously weakened in the HBO treatment group than in the simple ischemia group; At I/R 12 hours,neutrophils in the preoptic area and corpora striatum were significantly lower in the HBO treatment group than in the model group, respectively(P ＜ 0.05); At I/R 24 hours, neutrophils in the cerebral cortex, preoptic area and corpora striatum were significantly lower in the HBO treatment group than in the model group (P ＜ 0.05). ② Cerebrovascular leakage area was more significantly contracted in the HBO treatment group than in the model group (P＜ 0.05); At I/R 72 hours, the number of injured nerve cells in the optic chiasm cortex, medial area of corpora striatum and preoptic area was significantly smaller in the HBO treatment group than in the model group (P＜0.05). Neuronal damage was not found in the sham-operation group.CONCLUSION: HBO can markedly contract cerebrovascular leakage area of rats with acute focal cerebral ischemia/reperfusion injury, alleviate the symptoms of nervous system, inhibit neutrophilic infiltration and c-fos oncogene protein expression in the infarct area, and reduce neuronal necrosis in the "penumbral region".
