改良大鼠急性心肌梗死模型的制备方法

目的 探讨对大鼠急性心肌梗死模型方法进行改良的可靠性、稳定性及可重复性.方法 40只SD大鼠腹腔内注射苯巴比妥钠全身麻醉后,气管切开并插管,小动物呼吸机辅助呼吸.常规消毒铺巾后,切开左胸前区皮肤,经左侧第3、4肋间进入胸腔暴露心脏,明确左前降支冠状动脉后结扎造成急性心肌梗死.对围术期各种可导致结扎失败和死亡的原因进行分析.结果 成功建立了大鼠急性心肌梗死模型.术后24h大鼠存活率为95％,4w时存活率为92.5％.结论 通过方法改进能够快速有效建立大鼠急性心肌梗死模型并降低大鼠死亡率.     

降低大鼠心肌梗死模型死亡率的方法

目的 探讨降低大鼠心肌梗死模型死亡率的影响因素.方法 结扎180只Wistar雄性大鼠左冠状动脉前降支制备心肌梗死模型,分析麻醉药品、气管插管方法、结扎部位的高低及术后护理等因素对大鼠死亡率的影响,并取心脏组织行HE染色、氯化四唑（tetrazolium chloride,TTC）染色确认模型成功建立.结果 水合氯醛麻醉死亡率15%,戊巴比妥钠麻醉死亡率35%,差异有统计学意义（P＜0.05）;经口气管插管大鼠死亡率10%,经气管切开插管死亡率29.4%,差异有统计学意义（P＜0.05）;有术后护理大鼠死亡率5.9%,无术后护理大鼠死亡率22.2%,差异有统计学意义（P＜0.01）.而结扎部位的不同对大鼠手术死亡率及手术成功率亦有明显的影响.结论 本研究显示麻醉药品、气管插管方法、结扎部位的高低及术后护理等因素均对梗死模型的死亡率有影响,选择合适的麻醉药品和剂量以及气管插管方法,正确的结扎部位及适当的术后护理等可明显降低制作大鼠心肌梗死模型死亡率.     

建立大鼠急性心肌梗死模型方法的改良

目的:改良法建立大鼠心肌梗死的模型,提高造模成功率,减少死亡率。方法:60只清洁级SD大鼠,10%水合氯醛注射液腹腔注射麻醉。颈部小切口切开皮肤,暴露气管后利用导丝逆行牵拉技术进行气管插管。呼吸机辅助呼吸,左侧第4肋间进胸,交叉放置两开睑器充分暴露心脏,结扎冠状动脉左前降支。术毕利用注射器膨肺后关胸。4周后处死存活大鼠,取出大鼠心脏,行病理学检查。结果:术中死亡大鼠2只,术后第1天死亡1只,其余57只大鼠存活。4周后肉眼可见心脏标本梗死区心壁变薄,颜色变浅。镜下可见纤维组织排列紊乱、断裂、增生,炎性细胞浸润。提示57只大鼠建立心肌梗死模型成功,成功率93.3%。结论:利用改良法建立大鼠急性心肌梗死模型,死亡率低,造模成功率高。     

月龄及体重对急性心肌梗死大鼠室颤发生率的影响

目的 探讨月龄及体重对急性心肌梗死大鼠室颤发生率的影响.方法 选择2月龄、180～250 g SD大鼠(青年组),及15月龄、400～500 g SD大鼠(老年组)各20只为研究对象;采用开胸直视结扎法结扎大鼠左冠状动脉前降支引起大鼠急性心肌梗死,手术前后及手术过程中心电监护并记录心电活动,分析比较组间室颤等心律失常发生率.结果 在急性缺血性心肌梗死的SD大鼠模型中,老年组心律失常及室颤发生率显著高于成年组(心律失常发生率:85% vs 25%,P<0.01;室颤发生率55% vs 10%,P<0.01).结论 高月龄高体重老年大鼠急性心肌缺血后诱发室颤发生率明显高于低月龄低体重成年大鼠.     

大鼠慢性心肌梗死模型的制作

目的:建立可操作性强的大鼠慢性心肌梗死模型制作方法。方法:健康雄性SD大鼠40只采取开胸术式结扎冠状动脉前降支,观察结扎远端心肌颜色的改变和心电图变化确定是否梗死。结果:所有大鼠出现明确的梗死改变,心电图J点抬高,可出现Q波。早期死亡率为15%,总死亡率为22.5%。结论:准确结扎前降支才能保证造模成功,加强呼吸道管理是提高手术后大鼠成活率的重要措施。     

逆行牵引改良气管插管法提高大鼠心肌梗死模型成功率

目的研究采用逆行牵引改良气管插管法提高大鼠心肌梗死模型造模成功率的实验方法。方法 125只SD雄性大鼠,采用逆行牵引改良气管插管法(逆行插管组)和经口气管插管法(经口插管组)建立人工气道,结扎冠状动脉左前降支制作心肌梗死模型。4周后采用超声心动图检测大鼠心肌梗死模型心脏结构和心功能变化,采用Masson染色实验检测大鼠心脏胶原容积分数(CVF)。分析这两种气管插管方法、术中利多卡因的使用、手术操作过程中的细节问题、术中及术后护理事项等对大鼠模型成功率的影响。结果逆行牵引改良气管插管法建立大鼠人工气道的成功率为100%,明显高于传统的经口气管插管法(成功率为85%)。于左心耳与肺动脉圆锥连线下方2 mm进针结扎、结扎前滴1滴利多卡因到心脏表面减慢心率便于操作并预防心律失常、术中及术后及时清除气道分泌物、术中及术后保暖、预防伤口感染等方法,可提高大鼠心肌梗死模型的存活率。与正常大鼠比较,两组大鼠均出现左心室收缩末期内径变小,左心室后壁代偿性肥厚,左心室射血分数降低,心脏非心肌梗死区CVF增加;且两组间比较上述指标差异无统计学意义。逆行插管组心肌梗死模型造模成功率(76.7%)高于经口插管组(65.0%)。结论逆行牵引改良气管插管法的应用能够为大鼠心肌梗死模型的制作迅速备好人工气道,术中使用利多卡因、精准的血管结扎部位及合适的术中及术后护理对提高大鼠心肌梗死模型造模成功率具有重要意义。     

大鼠急性心肌梗死模型的建立

目的建立大鼠急性心肌梗死实验模型。方法采用戊巴比妥钠腹腔注射麻醉、直视下经口腔气管插管、开胸行冠脉左前降支结扎法,术后给予呼吸道管理;并进行心电图、心肌酶谱、病理组织学和坏死心肌组织学定量检查来证实。结果 40只模型组大鼠中,死亡6只,模型制备成功率85%。大鼠术后30 min,心电图肢体导联ST段弓背向上抬高,出现病理性Q波;结扎前降支血管后24 h和40 h时间点,模型组肌酸激酶同工酶、血清乳酸脱氢酶、乳酸脱氢酶同工酶较假手术组明显高,差异有统计学意义(P0.05),在60 h时间点血清乳酸脱氢酶、乳酸脱氢酶同工酶亦升高(P0.05);组织切片镜下观察病变区心肌细胞排列紊乱、疏松,细胞核固缩、碎裂;模型组心肌梗死与左心室湿重比值较假手术组明显高,差异有统计学意义(P0.01)。结论该心肌梗死动物模型构建方法简单,创伤轻,成功率高,结果可靠。     

经皮穿刺球囊封堵冠脉建立犬急性心肌梗死模型的实验研究

目的:探讨应用PTCA球囊封堵冠状动脉犬急性心肌梗死动物模型的实验方法。方法:选用杂种犬20只,麻醉后经股动脉置入PTCA球囊至左前降支（LAD）和左旋支（LCX）,封堵血流90min。结果:2只因指引导管致前降支闭塞发生心室纤颤死亡,2只因球囊封堵前降支近端约30min后发生心室纤颤死亡,4只在球囊拔除后发生心室纤颤死亡,1只封堵左旋支中段犬在心肌梗死后20h死亡。其余11只动物成功建立急性心肌梗死模型。前降支封堵术后1周,行超声心动图检查出现室间上部及前壁局部运动异常,室壁也变薄。结论:运用PTCA球囊封堵冠状动脉成功建立急性心肌梗死动物模型,可为研究提供较好的实验模型。     

开胸结扎犬冠状动脉建立急性心肌梗死动物模型的研究

无菌条件下,16只健康杂种犬全麻后,开胸暴露心脏,预阻断犬冠状动脉左前降支(LAD)第一对角支下距左主干1.5 cm处3次,5 min/次,后予结扎,应用结扎前后犬体内血清心肌酶的变化、心电图(ECG)改变、超声心动图(UCG)检查、病理组织切片等确定急性心肌梗死(AMI)模型建立情况.结果 16只健康杂种犬中,存活6周12只,存活1周1只,麻醉意外死亡1只,术中死于室颤2只.认为采用本文方法可成功制备AMI动物模型,简便易行,经济实用,术后可长期饲养.     

大鼠急性心肌缺血早期心电图QRS波群和ST段改变

目的利用大鼠心肌缺血模型,观察大鼠急性心肌缺血早期QRS波群和ST段变化及二者的关系。探讨大鼠缺血模型的成功标准。方法选用雄性SD大鼠108只,结扎左冠状动脉前降支制作大鼠心肌缺血模型。观察缺血5min内心电图QRS波群和ST段变化。结果①108只大鼠中,心肌缺血后R波明显增高89只(占82.4%),伴QRS波群时间增宽。②108只大鼠心肌缺血5minST段均有明显抬高,但5min内ST段改变过程表现为三种形式:缺血后ST段抬高过程中出现一过性下降,然后又逐渐抬高(60只,占55.6%);缺血后ST段抬高逐渐增加(37只,占34.3%);缺血后ST段先下降,1～5min后出现ST段抬高(11只,占10.2%)。③心肌缺血5min内QRS变化与ST段变化的关系:心肌缺血后R波明显增高的89只大鼠,其ST段出现上述三种改变,R波无明显变化的19只大鼠中,ST段变化均表现为缺血后抬高逐渐增加。R波增高越明显,QRS时间越宽,ST段下移也越明显。结论大鼠左冠状动脉前降支结扎后出现一过性R波增高、QRS波群增宽是心肌急性缺血损伤早期表现,在心电图记录中较ST段变化易于观察,可以作为早期结扎成功的心电图判断标准。     

普伐他汀对心肌梗死大鼠缝隙连接及室性心律失常的影响

目的:探讨大鼠心肌梗死(MI)时普伐他汀对室性心律失常的影响及其潜在的机制。方法:结扎大鼠冠状动脉前降支制备MI模型后随机分为假手术组(SO组,20只);MI组,25只;MI+普伐他汀组(MI-Pra组,25只),其中MI组和MI-Pra组分别用生理盐水和80mg/kg的普伐他汀喂养,每天2次,持续1周。给予程序性期前刺激诱发室性心律失常的发生,心电图监测室性心律失常。蛋白免疫印记法(Western blot)检测缝隙连接蛋白43(Cx43)的磷酸化蛋白及总量表达变化。免疫荧光观察Cx43表达分布情况。结果:MI组室性心动过速(室速)/心室颤动(室颤)诱发率(80.0%,20/25)较SO组(5.0%,1/20)明显增加(P<0.05);与MI组相比,MI-Pra组明显减少了MI导致的室速/室颤的发生(13.3%,6/25,P<0.05)。MI组Cx43的表达较SO组显著降低(P<0.05);与MI组相比,MI-Pra组Cx43的表达显著增高。免疫荧光结果显示,与SO组相比,MI组Cx43由端-端连接转化为侧-侧连接;与MI组相比,MI-Pra组Cx43分布紊乱明显改善。结论:普伐他汀能够显著减少MI大鼠室性...     

急性心肌梗死兔原发性心室颤动早期行心前区捶击复律效果探讨

目的：观察急性心肌梗死兔原发性心室颤动早期行心前区捶击复律的效果。方法：180只日本长耳兔,开胸结扎冠状动脉左旋支的左室支,制备急性心肌梗死模型。术中肢导联心电监护,将急性心肌梗死并发原发性心室颤动兔随机分为2组,实验组于2min内给心前区捶击,对照组给心脏按压。观察心室颤动转归。结果：心肌梗死造模过程中并发原发性心室颤动兔共15只,实验组8只行心前区捶击,5只成功转复为窦性心律,心前区捶击复律成功率62.5%。对照组7只采取心脏按压者均死亡,复律成功率为0%。2组差异显著（P〈0.05）。结论：急性心肌梗死兔原发性心室颤动早期行心前区捶击复律有效。     

冠心舒通胶囊对急性心肌梗死大鼠心功能作用的实验研究

目的 探讨冠心舒通胶囊对急性心肌梗死大鼠心功能的作用及其机制.方法 采用结扎大鼠左前降支的方法 制备急性心肌梗死大鼠模型,用1.4 F微导管和BL-420多道生理记录仪测量对照组、急性心肌梗死模型组及冠心舒通胶囊组左室压（LVP）及左室内压最大变速率（dp/dt）.结果 急性心肌梗死大鼠模型的心肌收缩力指标LVP和dp/dt明显低于正常对照组（P＜0.01,n=7）,而冠心舒通胶囊可明显改善心肌缺血大鼠心脏的血流动力学参数指标,并且有一定的剂量依赖性（P＜0.05,n=7）.结论 冠心舒通胶囊可以改善急性心肌梗死大鼠模型心功能.     

Vitamin E and ventricular fibrillation threshold in myocardial ischemia

The effect of vitamin E on the ventricular fibrillation threshold was studied in an experimental model of acute myocardial ischemia. An anterior thoracotomy was performed on 23 anesthetized Wistar rats. The ventricular fibrillation threshold was measured. Vitamin E was then administered intravenously to an experimental group (n = 11) and a placebo to a control group (n = 12). The ventricular fibrillation threshold was measured again. Finally, the left anterior descending coronary artery was occluded, producing anteroapical myocardial ischemia. The ventricular fibrillation threshold was measured again. This threshold did not vary significantly when vitamin E or the placebo was administered before occluding the coronary artery but after the occlusion a threshold decrease in the placebo group was observed, whereas no such decrease was manifested in the vitamin E-treated group. The results suggest that vitamin E prevents ventricular fibrillation in acute myocardial ischemia in rats.     

Complications of emergency coronary angioplasty for acute myocardial infarction]

To assess the incidence and consequences of complications occurring during emergency percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI), we studied 347 patients who underwent PTCA within 24 hours after the onset of AMI. Acute occlusion occurred in 29 patients (8.4%), of whom 16 patients underwent successful repeat PTCA. All of them survived until hospital discharge. The in-hospital reocclusion rates of these 16 patients were comparable to those of patients who had not experienced acute occlusion (18.8 vs 12.8%, ns). In the remaining 13 patients, reperfusion were not successful after acute occlusion, and 6 died. Side branch occlusion occurred in 21 patients (6.1%). Left circumflex artery occlusion occurring during PTCA for the proximal left anterior descending artery was fatal in 3 patients. Right ventricular branch occlusion during PTCA for the middle of the right coronary artery resulted in intractable right ventricular infarction in one patient, and he died. Among 14 patients who underwent repeat angiography, 13 had a patent side branch which had been occluded during PTCA. One patient had coronary rupture and died. During PTCA of the proximal left anterior descending artery, acute occlusion of the artery without reperfusion or occlusion of the left circumflex artery was often fatal. However, the prognosis of acute occlusion was relatively good, if repeat PTCA was successful and most of the occluded side branches remained patent in the chronic state.     

介入法置入栓塞弹簧圈制作猪急性心肌梗死模型

目的探讨介入法在猪冠状动脉内置入栓塞弹簧圈制作急性心肌梗死模型的可行性,建立一种新的急性心肌梗死模型方法。方法 26头中国实验用小型猪经股动脉穿刺,在前降支远段置入栓塞用弹簧圈(Cook公司产,型号:35-3-3),1周内观察心肌肌钙蛋白Ⅰ、心电图和冠状动脉造影,然后处死取出心脏,取目标冠状动脉和心肌,做病理学检查。结果术中2只死于造模过程中室颤,1只死于造模过程中出现麻醉意外,23头小型猪均发生了心肌梗死,且存活在1周以上,完成复查,总的成功率为88.5%。结论该模型制作具有操作简单、创伤小、死亡率低、成功率高等诸多优点,可作为较好的实验研究动物模型。     

Ventricular reentry and automaticity in myocardial infarction. Effect of size of injury

The effects of the size of acute myocardial infarction on ventricular reentry and automaticity were studied in 36 mongrel dogs. Large transmural myocardial infarctions were produced by ligation of the left anterior descending coronary artery (major ligation; diameter of infarction above 4.0 cm), and small subendocardial or intramural infarctions were produced by ligating a small diagonal branch of the left anterior descending coronary artery (minor ligation; diameter of infarction less than 1.5 cm). Reentrant arrhythmias were induced by rapid ventricular stimulation, and ventricular automaticity was determined during vagal stimulation. Ventricular automaticity became enhanced only 30 to 45 minutes after both major and minor coronary arterial ligations; however, the animals with major ligations attained a higher level of increased automaticity. While automaticity became enhanced in both groups reentrant arrhythmias could never be produced artificially (or observed spontaneously) in the animals with myocardial infarctions. The dependence of the so-called reentrant arrhythmias on the size of the infarction is a major support for the theory of reentry as the basis for these arrhythmias.     

Spontaneous and electrically induced ventricular arrhythmias during acute ischemia superimposed on 2 week old canine myocardial infarction

The arrhythmogenic effect of acute reversible myocardial ischemia before and 2 weeks after experimental myocardial infarction was investigated in 37 dogs that underwent reversible 10 min occlusion of the first major marginal branch of the left circumflex coronary artery. Subsequently, 24 of the dogs underwent experimental myocardial infarction with permanent left anterior descending coronary ligation, and 13 dogs served as sham-operated controls. Two weeks later, an open chest programmed electrical stimulation was performed in the 13 sham-operated and 24 postinfarction dogs to determine its accuracy in predicting the ventricular arrhythmias that develop during a subsequent episode of acute reversible ischemia. After programmed electrical stimulation, the left circumflex marginal branch was reversibly occluded for 10 min at the same site. The incidence of spontaneous ventricular fibrillation during reversible left circumflex marginal coronary occlusion did not differ from the first to the second study in sham-operated dogs, whereas in the postinfarction dogs, it increased from 13% before infarction to 54% after infarction (p = 0.005). The outcome of programmed electrical stimulation predicted spontaneous ventricular arrhythmias during coronary occlusion in only 21% of the postinfarction dogs. The accuracy of programmed electrical stimulation was 42% and its predictive value was 47% in detecting the dogs with spontaneous ventricular fibrillation. Regional myocardial blood flow measurements by microsphere technique identified the severity of reversible ischemia in the infarct border and periinfarction zones as a correlate of spontaneous ventricular fibrillation during coronary occlusion. In contrast, total infarct size correlated with electrically induced but not with spontaneous ventricular arrhythmias.     

Acute anterior wall infarct with intractable ventricular fibrillation: successful therapy by recanalization of a left anterior descending coronary artery occlusion

A 35-year-old male patient was admitted to the intensive care unit of a community hospital with an acute anterior myocardial infarction complicated by initial recurrent episodes of ventricular fibrillation and successful resuscitation. Persistent malignant ventricular arrhythmias during the following days necessitated external defibrillation approximately 250 times. The patient was transferred to the Hannover Medical School, where the occluded left anterior descending coronary artery was successfully recanalized. Eight days later, the malignant ventricular tachyarrhythmias ceased and after 59 days of hospitalization the patient could be discharged in stable condition.     

Cardiopulmonary bypass in a model of acute myocardial infarction and cardiac arrest

Cardiopulmonary bypass (CPB) reperfusion has demonstrated improved resuscitation rates in ventricular fibrillation cardiac arrest models. To investigate the effectiveness of CPB reperfusion in an ischemic cardiac arrest setting, simulating the clinical scenario of myocardial ischemia preceding sudden cardiac death, we developed a canine model of acute myocardial infarction followed by ventricular fibrillation. Sixteen dogs were randomly assigned to two groups. Group 1 (eight) had ventricular fibrillation induced without left anterior descending coronary artery occlusion. Group 2 (eight) had a thrombogenic copper coil placed in the left anterior descending artery and showed ECG evidence of acute myocardial infarction before induction of ventricular fibrillation. CPR commenced after eight minutes of ventricular fibrillation. Epinephrine 0.05 mg/kg and NaHCO3 1.0 mEq/kg were administered at ten minutes. CPB was begun at 12 minutes and continued for one hour. Myocardial ischemic and necrotic areas were determined in four-hour survivors by dual histochemical staining. All animals were resuscitated; all eight group 1 and six of eight group 2 animals survived to four hours. With the onset of CPB, coronary perfusion pressures increased significantly by 68.6 +/- 31.8 (SD) mm Hg in group 1 and 56.2 +/- 34.6 mm Hg in group 2 over those obtained with CPR (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)