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目的研究无创性延迟肢体缺血预适应(NDLIP)对心脏猝死的预防作用。方法取健康,体质量(250±10)g的SD♂大鼠30只,随机分为3组,1心肌梗死(MI)组:手术结扎动物冠状动脉左前降支(left anterior descending artery,LAD),2周后成模;2 MI+NDLIP组:动物心肌梗死模型成功后,每隔1 d进行1次远端肢体缺血预适应,直至第4周;3假手术(Sham)组:作为阴性对照组,心脏LAD只穿线不结扎,不实施NDLIP。各组动物常规饲养,于4周末静脉输注间羟胺(0.2 mg·min~(-1))进行猝死,记录致猝死过程中的ECG、猝死药物累积量、猝死时间,于猝死末期腹主动脉取血,ELISA法测定血清caspase-3、HSP70、SOD含量。结果间羟胺致动物心脏猝死时,随着给药量的增加,动物的心率呈下降趋势,记录给药0、5、10、30、50、70、90 min时动物的心率。与MI组相比,MI+NDLIP组给药0、5、10、30、50 min时动物心率[(479±8)vs(416±19)beat·min~(-1),(446±32)vs(370±20)beat·min~(-1),(376±53)vs(305±29)beat·min~(-1),(307±63)vs(244±33)beat·min~(-1),(283±45)vs(121±35)beat·min~(-1),P<0.01]明显较高。与MI组相比,MI+NDLIP组动物的致猝死药物累积量、猝死时间[(14.58±3.03)vs(10.76±2.73)mg,(72.9±15.2)vs(53.8±13.6)min,P<0.01]都明显增加。与MI组相比,MI+NDLIP组血清caspase-3[(2.01±0.52)vs(2.34±0.38)μg·L~(-1),P<0.01]表达量明显降低;HSP70[(3.01±0.58)vs(2.70±0.43)μg·L~(-1),P<0.05]水平明显升高;SOD[(1.99±0.65)vs(1.70±0.58)mg·L~(-1),P<0.01]水平明显升高。结论无创性延迟肢体缺血预适应能有效预防大鼠心梗后心脏性猝死,其机制可能与降低心肌细胞凋亡、增加保护性蛋白的表达以及增强心肌抗氧化能力有关。
Objective To study the preventive effect of noninvasive delayed limb ischemic preconditioning (NDLIP) on sudden cardiac death. Methods Thirty SD SD rats with healthy body weight (250 ± 10) g were randomly divided into 3 groups: 1 myocardial infarction (MI) group: left anterior descending artery (LAD) , 2 weeks after modeling; 2 MI + NDLIP group: animal models of myocardial infarction success 1 d distal ischemic preconditioning every 1 d, until the first 4 weeks; 3 Sham group: as a negative control group , Heart LAD threading only do not ligate, do not implement NDLIP. Animals in each group were routinely housed, and were killed suddenly by intravenous injection of hydroxylamine (0.2 mg · min -1) at the end of 4 weeks. The ECG of sudden death, sudden drug accumulation and sudden death were recorded. At the end of sudden death, abdominal aorta Blood samples were taken for determination of serum caspase-3, HSP70 and SOD by ELISA. Results During the sudden cardiac death of hydroxylamine-induced animals, the heart rate of the animals showed a decreasing trend with the increase of the dose, and the heart rate of the animals at 0, 5, 10, 30, 50, 70 and 90 minutes was recorded. Compared with MI group, heart rate of animals in MI + NDLIP group at 0, 5, 10, 30, 50 min (479 ± 8 vs 416 ± 19) beat · min ~ (-1), (446 ± 32) (370 ± 20) beat · min ~ (-1), (376 ± 53) vs (305 ± 29) beat · min ~ (-1), (307 ± 63) vs (244 ± 33) ~ (-1), (283 ± 45) vs (121 ± 35) beat · min ~ (-1), P <0.01] Compared with the MI group, the cumulative amount of sudden death and the time of sudden death in the MI + NDLIP group [(14.58 ± 3.03) vs (10.76 ± 2.73) mg, (72.9 ± 15.2 vs 53.8 ± 13.6) min, P <0.01 ] Are significantly increased. Compared with MI group, the expression of caspase-3 [(2.01 ± 0.52) vs (2.34 ± 0.38) μg · L -1, P <0.01] in MI + NDLIP group was significantly lower than that in MI group (2.70 ± 0.43) μg · L -1, P <0.05]. SOD (1.99 ± 0.65) vs (1.70 ± 0.58) mg · L -1, P <0.01 ] Levels were significantly higher. Conclusions Noninvasive delayed limb ischemic preconditioning can effectively prevent sudden cardiac death after myocardial infarction in rats. The mechanism may be related to the decrease of myocardial apoptosis, the increase of protective protein expression and the enhancement of myocardial antioxidant capacity.