中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2009年
46期
9032-9036
,共5页
背景:国外20世纪90年代开始采用球囊封堵建立闭胸式心肌梗死动物模型,但术中室颤及血栓形成等因素降低了制作心肌梗死动物模型的成功率.目前国内建立球囊封堵闭胸式心肌梗死大动物模型的报道较少.目的:应用球囊封堵法建立闭胸式猪心肌梗死模型,探索提高建模成功率的方法.设计、时间及地点:随机对照动物实验,病理观察,于2008-07/2009-05在昆明医学院第一附属医院心内科及昆明医学院病理教研室完成.材料:8～11月龄健康滇南小耳猪15只,体质量19～25kg,随机数字表分为3组:假手术组、缺血再灌注组、缺血后处理组,每组5只.方法:冠脉封堵后和再灌注期预防性静滴利多卡因1.0～2.0mg/kg,以减少恶性心律失常的发生率,使用肝索防治血栓形成,在X射线监控下将球囊导管送至冠状动脉左前降支第一对角支的远端,假手术组只放置球囊至冠状动脉左前降支,不封堵;缺血再灌注组行球囊充气堵闭冠状动脉左前降支60min后撤除球囊:缺血后处理组行球囊充气堵闭冠状动脉左前降支60min后,球囊放气30s,充气30s(循环8次)后撤除球囊.主要观察指标:行冠脉造影、心电图及心肌酶检测评价心肌梗死模型的建立情况.3d后行心肌三氯四氮唑染色及病理学检查验证心肌梗死.结果:假手术组猪全部存活;缺血再灌注组4只成功建立心肌梗死模型,1只死于顽固性室颤;缺血后处理组全部成功建立心肌梗死模型.堵闭左前降支远端后,心电图V1～3导联上ST段抬高,有病理性Q波形成:心肌酶谱演变过程与人体心肌梗死过程基本一致.心肌梗死部位分别位于心尖、左心室前壁、前间隔部.三氯四氮唑染色后正常心肌呈砖红色,梗死区心肌颜色暗淡,呈灰白色;病理学检查显示,梗死区心肌正常结构破坏,胞浆浓缩,染色加深,横纹消失,核浓缩、溶解、碎裂,梗死区内有较多的红细胞,梗死区周围有较多肉芽组织增生及大量炎性细胞浸润.结论:球囊封堵冠脉建立猪闭胸式心肌梗死模型对动物创伤性小,且最为接近临床实际的过程,术中使用利多卡因及肝素防治心律失常及血栓形成是成功建立该模型的有效方法,缺血后处理可能是提高建模成功率的因素之一.
揹景:國外20世紀90年代開始採用毬囊封堵建立閉胸式心肌梗死動物模型,但術中室顫及血栓形成等因素降低瞭製作心肌梗死動物模型的成功率.目前國內建立毬囊封堵閉胸式心肌梗死大動物模型的報道較少.目的:應用毬囊封堵法建立閉胸式豬心肌梗死模型,探索提高建模成功率的方法.設計、時間及地點:隨機對照動物實驗,病理觀察,于2008-07/2009-05在昆明醫學院第一附屬醫院心內科及昆明醫學院病理教研室完成.材料:8～11月齡健康滇南小耳豬15隻,體質量19～25kg,隨機數字錶分為3組:假手術組、缺血再灌註組、缺血後處理組,每組5隻.方法:冠脈封堵後和再灌註期預防性靜滴利多卡因1.0～2.0mg/kg,以減少噁性心律失常的髮生率,使用肝索防治血栓形成,在X射線鑑控下將毬囊導管送至冠狀動脈左前降支第一對角支的遠耑,假手術組隻放置毬囊至冠狀動脈左前降支,不封堵;缺血再灌註組行毬囊充氣堵閉冠狀動脈左前降支60min後撤除毬囊:缺血後處理組行毬囊充氣堵閉冠狀動脈左前降支60min後,毬囊放氣30s,充氣30s(循環8次)後撤除毬囊.主要觀察指標:行冠脈造影、心電圖及心肌酶檢測評價心肌梗死模型的建立情況.3d後行心肌三氯四氮唑染色及病理學檢查驗證心肌梗死.結果:假手術組豬全部存活;缺血再灌註組4隻成功建立心肌梗死模型,1隻死于頑固性室顫;缺血後處理組全部成功建立心肌梗死模型.堵閉左前降支遠耑後,心電圖V1～3導聯上ST段抬高,有病理性Q波形成:心肌酶譜縯變過程與人體心肌梗死過程基本一緻.心肌梗死部位分彆位于心尖、左心室前壁、前間隔部.三氯四氮唑染色後正常心肌呈磚紅色,梗死區心肌顏色暗淡,呈灰白色;病理學檢查顯示,梗死區心肌正常結構破壞,胞漿濃縮,染色加深,橫紋消失,覈濃縮、溶解、碎裂,梗死區內有較多的紅細胞,梗死區週圍有較多肉芽組織增生及大量炎性細胞浸潤.結論:毬囊封堵冠脈建立豬閉胸式心肌梗死模型對動物創傷性小,且最為接近臨床實際的過程,術中使用利多卡因及肝素防治心律失常及血栓形成是成功建立該模型的有效方法,缺血後處理可能是提高建模成功率的因素之一.
배경:국외20세기90년대개시채용구낭봉도건립폐흉식심기경사동물모형,단술중실전급혈전형성등인소강저료제작심기경사동물모형적성공솔.목전국내건립구낭봉도폐흉식심기경사대동물모형적보도교소.목적:응용구낭봉도법건립폐흉식저심기경사모형,탐색제고건모성공솔적방법.설계、시간급지점:수궤대조동물실험,병리관찰,우2008-07/2009-05재곤명의학원제일부속의원심내과급곤명의학원병리교연실완성.재료:8～11월령건강전남소이저15지,체질량19～25kg,수궤수자표분위3조:가수술조、결혈재관주조、결혈후처리조,매조5지.방법:관맥봉도후화재관주기예방성정적리다잡인1.0～2.0mg/kg,이감소악성심률실상적발생솔,사용간색방치혈전형성,재X사선감공하장구낭도관송지관상동맥좌전강지제일대각지적원단,가수술조지방치구낭지관상동맥좌전강지,불봉도;결혈재관주조행구낭충기도폐관상동맥좌전강지60min후철제구낭:결혈후처리조행구낭충기도폐관상동맥좌전강지60min후,구낭방기30s,충기30s(순배8차)후철제구낭.주요관찰지표:행관맥조영、심전도급심기매검측평개심기경사모형적건립정황.3d후행심기삼록사담서염색급병이학검사험증심기경사.결과:가수술조저전부존활;결혈재관주조4지성공건립심기경사모형,1지사우완고성실전;결혈후처리조전부성공건립심기경사모형.도폐좌전강지원단후,심전도V1～3도련상ST단태고,유병이성Q파형성:심기매보연변과정여인체심기경사과정기본일치.심기경사부위분별위우심첨、좌심실전벽、전간격부.삼록사담서염색후정상심기정전홍색,경사구심기안색암담,정회백색;병이학검사현시,경사구심기정상결구파배,포장농축,염색가심,횡문소실,핵농축、용해、쇄렬,경사구내유교다적홍세포,경사구주위유교다육아조직증생급대량염성세포침윤.결론:구낭봉도관맥건립저폐흉식심기경사모형대동물창상성소,차최위접근림상실제적과정,술중사용리다잡인급간소방치심률실상급혈전형성시성공건립해모형적유효방법,결혈후처리가능시제고건모성공솔적인소지일.
BACKGROUND:In 1990s,overseas researchers use balloon occlusion method for establishing closed-chest animal models of myocardial infarction. But,ventricular fibrillation and thrombosis of intraoperative factors reduce the success rate of establishing the models. Currently,there are a few reports on establishing the large animal models. OBJECTIVE:We used balloon occlusion method for establishing closed-chest swine models of myocardial infarction,and explored ways to improve the success rate of modeling. DESIGN,TIME AND SETTING:The randomized controlled animal study of pathology observation was performed at the Department of Cardiology,First Affiliated Hospital of Kunming Medical College and Research Room of Pathology,Kunming Medical College from July 2008 to May 2009. MATERIALS:Fifteen Diannan small-ear pigs weighing 19-25 kg,aged 8-11 months,were divided into three groups:sham operation group,ischemia-reperfusion group,and ischemic postconditioning group,with 5 pigs in each group.METHODS:After the coronary occlusion and reperfusion period,the prophylactic use of lidocaine (1.0-2.0 mg/kg) infusion to control arrhythmia,and use of heparin to prevent and treat the thrombosis. A balloon catheter was positioned in the distal end of the first diagonal branch of the left anterior descending (LAD) artery under fluoroscopic guidance. In the sham operation group,the balloon was only placed to the LAD,did not block coronary artery. In the ischemia-reperfusion group,inflatable balloon occlusion was done for 60 minutes in the LAD after the balloon removed. In ischemic postconditioning group,after the balloon was inflated and occluded the LAD for 60 minutes,ischemic postconditioning was elicited by eight cycles of 30-second reperfusion,followed by 30-second reocclusion.MAIN OUTCOME MEASURES:Coronary angiography,electrocardiogram (ECG) and cardiac enzymes test was conducted to evaluate models of myocardial infarction. After three days,cardiac 2,3,5-triphenyltetrazolium chloride (TTC) staining and pathological examination was done to verily myocardial infarction.RESULTS:In the sham operation group,all pigs survived. In the ischemia-reperfusion group,4 pig models of myocardial infarction were successfully established,and one died of refractory ventricular fibrillation. In the ischemic postconditioning group,models of myocardial infarction after ischemia were successfully established. Following distal left anterior descending artery occlusion,the ECG leads V13 on the ST-segment elevation,the sick rational Q-wave formed;myocardial enzyme evolution of myocardial infarction in the human body was basically the same process. The site of myocardial infarction,basically the same parts,was located in apical,left ventricular anterior wall,and the former interval. TTC staining was normal myocardium brick red,myocardial infarct area appeared pale;pathological examination revealed a normal structure of myocardial infarct damage,cytoplasm condensed,dyeing deepening,transverse striations disappeared,nuclear enrichment,dissolution,fragmentation,many erythrocytes around the infarct area with abundant granulation tissue and a large infiltration of inflammatory cells.CONCLUSION:The described model presents a less invasion to the animals,and is the closest to the process of clinical practice.Intraoperative use of lidocaine and heparin for controlling arrhythmia and thrombosis of the models is successfully established as an effective manner. Ischemic postconditioning may be one of the factors for improving the modeling success rate.
