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AIM:To establish the rat model of ischemic chronic heart failure by coronary artery ligation combining with exhaustive swimming.METHODS:40 adult rats were treated with coronary artery ligation,after 4 weeks cardiac function measurement were conducted by ultrasonography.Rats with LVEF below 40％ are considered as successful model duplication.11 rats were collected for the coronary artery ligation group,while the rest (whose LVEF were bigger than 40％) were pushed to swim for 1h per day by 15 days to promote the model formation which 8 rats were collected for exhaustion with ligation group.Left ventricular function indexes,brain natriuretic peptide (BNP) and cardiac histomorphologic changing were checked,and compared with the Control group (10 rats).RESULTS:LVEF of exhaustion with ligation group was (38.70 ± 10.10) ％,coronary artery ligation group (39.20 ± 11.10)％,which was obviously decreasing (P ＜ 0.01) compared with that of the control group (84.60 ± 3.64) ％.LVEDP of exhaustion with ligation group was (11.5 ± 1.3) mm Hg,coronary artery ligation group [(10.68 ± 4.45)mm Hg],which was obviously increasing (P ＜ 0.01)compared with that of the Control group [(4.4 ± 0.2) mm Hg].The BNP level of exhaustion with ligation group was (561.0 ± 21.0) μg/L,coronary artery ligation group (548.6 ± 25.8) μg/L,which was obviously increasing (P ＜0.01) compared with that of control group [(366.2 ± 21.8) μg/L].There are lots of red myocardial cells with stripe clear in the control group based on Masson's trichrome staining,but there are so many blue collagenous fibers instead of myocardial cells in exhaustion with ligation group and coronary artery ligation group.The standard-reaching rate of model was about 35％ at 4 weeks after operation,while final standard-reaching rate rose to about 62％ after exhausting swimming.Although the difference between the indexes of the coronary artery ligation group and the post ligation group was not significant,the rate of improvement was significant (P ＜ 0.01).CONCLUSION:Ligation of coronary artery combined with swimming exhaustion can establish ischemic chronic heart failure model,which is more economic and can obtain high success rate,thus is suitable to generalization.
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Acute myocardial infarction is one of the major causes of death in the world. Research on animal models of myocardial infarction has a great significance in improving the pathophysiology, diagnosis and treatment of human myocardial infarction. At present, problems such as low survival rate and complicated preparation still exist. In recent years, some progress has been made in the preparation of animal myocardial infarction models, which can improve the survival rate, qualified rate and speed. This paper analyzes the preparation of rat models of acute myocardial infarction and related research, combined with actual factors to simplify the process of preparation and improve the skills of scientific researchers, so as to provide a source of stable and reliable acute myocardial infarction models for medical research.
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Acute myocardial infarction is one of the major causes of death in the world. Research on animal models of myocardial infarction has a great significance in improving the pathophysiology, diagnosis and treatment of human myocardial infarction. At present, problems such as low survival rate and complicated preparation still exist. In recent years, some progress has been made in the preparation of animal myocardial infarction models, which can improve the survival rate, qualified rate and speed. This paper analyzes the preparation of rat models of acute myocardial infarction and related research, combined with actual factors to simplify the process of preparation and improve the skills of scientific researchers, so as to provide a source of stable and reliable acute myocardial infarction models for medical research.
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Objective To investigate the protective effects and mechanism of TG 6 on myocardial ischemia/reperfusion injury . Methods the protective effects of TG 6 on myocardial ischemia/reperfusion was investigated by setting up models of ischemia and reperfusion of rats induced by ligating the left coronary anterior descending artery in vivo,isolated rat hearts through an improved Lange-ndorff device, and hypoxia /reoxygenation injury of neonatal rat cardiomyocytes , and the serum CK,LDH,T-SOD, MDA were taken as research markers .Results TG6 significantly reduced the myocardial infarct size , decreased the activity of CK and the content of MDA in serum, reduced the activity of LDH, and increased the activity of T-SOD in vivo;TG6 obviously increased the coronary blood flow after low rate perfusion and reperfusion , decreased the content of MDA and the leakage of CK , LDH in myocardial tissue , elevated the activity of T-SOD in vitro of isolated rat hearts;TG6 had no effects on cells in normal growth condition , raised the viability of cardio-myocytes significantly, and reduced the rate of CK leakage and the content of [Ca2+]i obviously in Na2S2O4 treated cells in vitro of neonatal rat cardiomyocytes .Conclusion TG6 could effectively protect myocardial ischemia/reperfusion injury .
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Objective To observe the effects of Dl-3-n-butylphthalide ( NBP) on the mitochondria infarction, size of myocardial infarction and myocardial apoptosis after acute myocardial ischemia in rats. Methods 92 male SD rats were divided into sham operation group (8 rats) , model group (21 rats) , and low-dose NBP group (21 rats) , medium-dose NBP group (21 rats) , high-dose NBP group (21 rats) . The model and NBP groups were made into MI model by ligation of the left anterior descending ( LAD) coronary artery, but not in sham-operated group. Model group and NBP group were taken heart specimens after coronary artery ligation. Cardiomyocyte apoptosis was ana-lyzed by TUNEL in each group. Size of MI was analyzed by TTC staining in sham-operated group, model group and high-dose NBP group. Electron perspective microscopy was applicated in observing mitochondria infarction in model group and high-dose NBP group after myocardial infarction. The expressions of Bcl-2 protein and Bax protein were detected by Western blot. Results Compared with model group, butylphthalide significantly increased expression of Bcl-2 protein ( P <0.05 ) and the ratio of Bcl-2/Bax ( P <0.05 ) , inhibited mitochondria infarction ( P <0.05 ) , reduced myocardial infarct size ( P<0.01 ) and cardiomyocyte apoptosis ( P<0.05 ) . Conclusion Bu-tylphthalide significantly inhibits myocardial infarction by increasing expression of Bcl-2 protein and the ratio of Bcl-2/Bax and decreasing mitochondria infarction, reducing myocardial infarct size and cardiomyocyte apoptosis in rats during the acute myocardial ischemia process.
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AIM: To observe protective effects of sanguis draxonis flavones on myocardial ischemia in rats and dogs. METHODS: Acute myocardial ischemia in rats was produced by iv pituitrin and ECG indexes were observed. Myocardial ischemia was induced by ligating coronary artery in anaesthetized dogs, and then EEC, CK,LDH, and LD in serum were determined respectively. RESULTS: J point and T wave in rats changed evidently after iv pituitrin, which was reversed by sanguis draxonis flavones (360, 180 mg?kg~ -1). In coronary artery ligation model, infraction range, △N-ST, △?-ST and some serum indexes (such as CK, LDH and LD) was decreased after ig sanguis draxonis flavones (120, 60, 30 mg?kg~ -1). CONCLUSION: Acute myocardial ischemia is protected effectively by sanguis draxonis flavones.
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In order to observe the change of epicardial ECG(Eep), left ventricular pressure, left ventricular dp/dt and the development of arrhythmia during regional myocardial ischemia and reperfusion, proximal LAD was ligated for 30 minutes and reperfused suddenly for 30 minytes in eleven mongrel dogs which were grouped into control(n=6) and diltiazem(n=5) group. In diltiazem group, diltiazem infusion was started 10 minutes prior to reperfusion with the speed of 0.02mg/kg/min for 25 minutes. The amount of injury current was measured from TQ segment and ST segment changes of Eep, and its effect on the incidence of reperfusion arrhythmia was evaluated. Eep, LV pressure, LV dp/dt and ECG were simultaneously recoreded with the paper speed of 100mm/sec at predetermined time intervals, and 6 channel ECG(standard lead I, II, III, AVR, AVL, AVF) was recorded continuously with paper speed of 10mm/sec throughout the experiment. The results were as follows ; 1) After ligation of LAD, the polarity QRS of Eep changed to show monophasic shape from 3-4 minutes, TQ segment depressed to reach minumum level at 4-7 minutes and ST segment elevated to reach maximum level at 4-5 minutes. These changes recovered rapidly to pre-ligation state after reperfusion, and this tendency was not affected by diltiazem. 2) The absolute value of LV dp/dt max and LV dp/dt min decreased 10% at 2-4 minutes after LAD ligation, and began to recover from 7 minutes after reperfusion to reach peak recovery value at 20 minutes after reperfusion in control group. In diltiazem group, it decreased 15% after diltiazem infusion and began to recover from 1 minutes after reperfusion to reach peak recovery value at 7 minutes after reperefusion. 3) Ischemic ventricular fibrillation was observed at the time of maximum TQ depression and ST segment elevation and 4 out of 6 events were developed within 5 minutes after LAD ligation. The cases with Isch-Vf developed Rep-Vf without exception, which was observed in 8 out of 11 cases and was noted within 1 minutes after reperfusion except one. 4) Maximum ST elevation was significantly higher in group with Rep-Vf then in group without Rep-Vf(Rep-Vf(+);18.5+/-11.1, Rep-Vf(-);10.3e+/-6.9, p<0.05), and also maximum ST elevation was significantly higher in group with both Isch-Vf and Rep-Vf then in group with only Rep-Vf(Isch-Vf+Rep-Vf;28.5+/-7.8, Rep-Vf only;10,5+/-4.7, P<0.01). 5) The incidende of reperfusion ventricular fibrillation was 83% in control group(5 out of 6) and 60% in diltiazem group(3 out of 5), but the inhibitory effect of diltiazem on the reperfusion Vf could not be confirmed due to the difference of the incidence of ischemic Vf between the two groups(control group;67%(4 out of 6), ditiazem group;20%(1out of 5)). In conclusion, maximum injury current developed 4-7 minutes after coronary artery ligation, and maximum ST elevation value was significantly related with the development of ischemic Vf and reperfusion Vf, and the inhibitory effect of diltiazem on the reperfusion ventricular fibrillation could not be confirmed in this study.
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Animals , Dogs , Arrhythmias, Cardiac , Coronary Vessels , Depression , Diltiazem , Electrocardiography , Incidence , Ligation , Myocardial Ischemia , Reperfusion , Ventricular Fibrillation , Ventricular PressureABSTRACT
Objective To investigate the effects of different ligation position,vena coronaria variation and lidocaine on myocardial infarction size and mortality in rats Methods Totally 120 male SD rats were divided into four groups with 30 rats in each group: low ligation with invisible vena coronaria,low ligation with visible vena coronaria,high ligation,and high ligation plus lidocaine Results MI was successfully created in 930% rats of high ligation groups and in 673% rats of low ligation groups The mortality was 433% in rats of high ligation groups,only 133% in rats when lidocaine in use Conclusion High ligation increases the success rate of rat model of myocardial infarction and the application of lidocaine decreases the mortality of the rat model