| Objective:(1) To study the effect of noninvasive delay distal limb ischemia preconditioning(NDLIP) on animal cardiac function, myocardial morphology and myocardial metabolism after prognosis of myocardial infarction.(2) To research the effect of movement on animals after NDLIP.(3) To research NDLIP preventive effect of NDLIP on sudden cardiac death.Methods:(1) Take 45 healthy SD male rats with weight 250±10g and randomly divide into 3 groups, ①Myocardial Infarction(MI) group: make surgical ligation of animal LAD, then become model after two weeks. ②Noninvasive delay distal limb ischemia preconditioning(NDLIP) group: after the success of the myocardial infarction animal model, make distal limb ischemia preconditioning every other day until 4 weeks, 6 weeks and 8 weeks later. ③Sham group: as the negative control group, take heart LAD threading and not implement ligation on it.Feed animals conventionally, make ventricular intubation, monitor hemodynamic parameters at the end of the 4, 6, 8 weeks, then get blood from abdominal aorta,measure Bcl-2, CK-MB, Bax and c Tn I with ELISA method; get left ventricular anterior wall and uniform it, as well as measure myocardial tissue of mitochondrial respiratory chain complexes Ⅰ, Ⅱ, Ⅲ, Ⅳ with ELISA method(2) take 60 healthy SD male rats with weight 250±10 g and randomly divide into 4 groups, and the disposal method of ①~③ groups to is same to(1); ④ NDLIP + exercise group:after the success of the myocardial infarction animal model, make distal limb ischemia preconditioning every other day until 4, 6, 8 weeks, then give a certain intensity exercise for a week; feed animals conventionally, get left ventricular anterior wall and uniform it at the end of the 4, 6, 8 weeks; measure myocardial tissue ATP and NOS enzyme activity with ELISA method; measure cell apoptosis rate with TUNEL method.(3) Take 30 healthy SD male rats with weight 250±10 g and randomly divide into 3 groups as same as(1); give 4 groups of rats a sudden death with metaraminol bitartrate at the end of 4 weeks, record ECG in the process of sudden death, drug cumulant of sudden death, and death time; get blood fromabdominal aorta at the end of the sudden death; measure Caspase- 3, HSP70 and SOD activity with ELISA method.Results:1. The effect of NDLIP on hemodynamic parameters at 4, 6, 8 weeks after LAD ligation.After myocardial infarction, at 4, 6, 8 weeks, compared with MI group,hemodynamic index of NDLIP group has improved. Left ventricular systolic pressure(105.72±5.46, 112.13±4.19 and 4.19±1.32 vs 91.51±1.74, 93.37±6.76 and6.76±6.90 mm Hg, P<0.05) significantly increased; left ventricular end-diastolic pressure(16.98±5.59, 5.59±5.24 and 16.32±5.63 vs 29.35±5.40, 26.51±5.02 and5.02±4.95 mm Hg, P<0.05) significantly decreased.2. Influence of NDLIP on mitochondrial respiratory chain complexes Ⅰ, Ⅱ,Ⅲ, Ⅳ at 4, 6, 8 weeks after myocardial infarction.After myocardial infarction, at 4, 6, 8 weeks, compared with MI group,mitochondrial respiratory chain complexⅠof NDLIP group(11.94±1.35, 12.66±4.29 and 4.29±1.54 vs 6.77±2.39, 6.62±2.15 and 2.15±1.71 ng/ml, P<0.01), mitochondrial respiratory chain complexesⅡ(9.79±2.31, 10.60±3.17 and 3.17±5.06 vs 5.47±2.35,6.46±2.70 and 2.70±0.94 ng/ml, P<0.05), mitochondrial respiratory chain complexesⅢ(3.67±1.79, 5.76±1.79 and 1.79±1.36 vs 1.61±0.51, 3.55±1.67 and 1.67±0.37ng/ml, P<0.05), mitochondrial respiratory chain complexes Ⅳ(2.08±0.59,2.73±1.04 and 1.04±1.39 vs 1.37±0.25, 1.69±0.44 and 0.44±0.31 ng/ml, P<0.05)were significantly increased.3. The effect of NDLIP on Bcl-2, Bax expression at 4, 6, 8 weeks after myocardial infarction.After myocardial infarction, at 4, 6, 8 weeks, compared with MI group, serum Bcl-2 of NDLIP group(126.85±17.78, 121.84±13.85 and 13.85±18.12 vs318.65±61.98, 367.53±50.38 and 50.38±51.08 pg/ml, P<0.01) were significantly reduced and Bax level increased remarkably(162.47±21.37, 263.24±18.77 and18.77±39.27 vs 113.85±10.57, 145.82±35.64 and 35.64±21.34 pg/ml, P<0.05).4. The effect of NDLIP on CK-MB, c Tn I at 4, 6, 8 weeks after myocardial infarction.After myocardial infarction, at 4, 6, 8 weeks, compared with MI group, serum CK-MB levels(28.73±4.89, 26.42±5.72 and 24.15±6.25 vs89.06±24.57, 112.98±25.62 and 79.52±27.21 ng/ml, P<0.01) were significantly reduced and c Tn I levels(3.39±0.70, 2.98±0.32 and 3.25±0.73 vs 6.32 ± 1.20,7.16±1.28 and 11.13±2.22 ng/ml, P<0.01) also decreased remarkably.5. Take exercise and NDLIP for prognosis of myocardial infarction in animals and monitor the impact on the myocardial cell apoptosis with TUNEL method.After myocardial infarction for animal, make NDLIP intervention firstly, take movement with a certain intensity subsequently. Compared with MI group,myocardial apoptosis index of NDLIP group(80.45±5.58, 70.00±4.73 and76.43±4.91 vs 90.32 ±4.65, 95.83±3.59 and 3.59±13.90%, P<0.05) significantly reduced, the myocardial apoptosis index of NDLIP + exercise group(88.07±1.87,87.21±4.75 and 4.75±5.42 vs 90.32±4.65, 95.83±3.59 and 3.59±13.90%, P<0.05)also decreased remarkably, but NDLIP group reduced more; compared NDLIP group with NDLIP + exercise group, P<0.05.6. The effect of exercise and NDLIP on myocardial ATP levels at 4, 6, 8 weeks after LAD ligation for the prognosis of myocardial infarction.After myocardial infarction for animal, make NDLIP intervention first, take excerise with a certain intensity subsequently. Compared with MI group, ATP levels of NDLIP group(50.80±0.63, 54.96±0.45 and 41.96±0.44 vs 26.77±0.73, 22.19±0.36 and 20.58±0.58 ng/ml, P<0.01) increased significantly and ATP of NDLIP+ exercise group(42.71±0.40, 44.73±0.31 and 40.36±0.28 vs 26.77±0.73, 22.19±0.36 and20.58±0.58 ng/ml, P<0.01) also increased remarkably, but NDLIP group increased more; compared NDLIP group with NDLIP + exercise group, P<0.05.7. The effect of exercise and NDLIP on NOS enzyme levals at 4, 6, 8 weeks after LAD ligation for the prognosis of myocardial infarction in animals.After myocardial infarction for animal, make NDLIP intervention first, take movement with a certain intensity subsequently. Compared with MI group, NOSlevels of NDLIP group(9.24±5.07, 14.07±2.11 and 22.38±4.51 vs 13.55±5.31,21.60±8.51 and 28.10±2.44 ng/ml, P<0.01)reduced remarkably and NOS levels of NDLIP + exercise group also decreased significantly, but NDLIP group decreased more; compared NDLIP group with NDLIP + exercise group, P<0.05.8. The effect of NDLIP on physiological indexes of heart, death time and death drug accumulative dose in the process of sudden death.While metaraminol bitartrate lead animal cardiac sudden death, with the increase of dosage, the animal’s heart rate is declining; record animal’s heart rate before the sudden death, for 5, 10, 30, 50, 70, 90 min; compared with the MI group,animal death heart rate of NDLIP group(479±8 vs 416±19 beat/min, P<0.01) are significantly higher. After dosing of NDLIP group for 5, 10, 30, 50 minintes, animal heart rate(446±32 vs 370±20 beat/min, 376±53 vs 305±29 beat/min, 307±63 vs244±33 beat/min, 283±45 vs 121±35 beat/min, P<0.01) significantly higher.Compared with MI group, animal drugs cumulant to sudden death, death time of NDLIP group(14.58±3.03 vs 10.76±2.73 mg, 105.4±3.9 vs 53.8±13.6 min, P<0.01)increased significantly.9. The effect of NDLIP prevention of sudden cardiac death on expression of Caspase 3, HSP70, SOD.While metaraminol bitartrate lead animal cardiac sudden death, compared with MI group, serum Caspase-3 expression quantity(2.01±0.52 vs 2.34±0.38ng/ml,P<0.01) significantly reduced; HSP70 levels(3.01±0.58 vs 2.70±0.43ng/ml, P<0.01)increased remarkably SOD levels(1.99±0.65 vs 1.70±0.58ng/ml, P<0.01) increased significantly.Conclusion:1. Implementing NDLIP after myocardial infarction can improve the hemodynamic indexes, promote the mitochondrial respiratory function, inhibiting cell apoptosis thus improve the prognosis.2. For rats in myocardial infarction, implementing NDLIP firstly then taking a certain intensity exercise also has a certain improvement on its prognosis, but not better than the single implementation of NDLIP.3. NDLIP can prevent sudden cardiac death after myocardial infarction in rats through reducing the myocardial cell apoptosis, increasing protective protein expression and enhancing antioxidant capacity. |
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