大鼠心肌缺血再灌注损伤中钙调神经磷酸酶的活性研究

发布时间：2018-08-02 18:53

【摘要】：钙调神经磷酸酶(Calcineurin,CaN)是迄今发现的唯一受Ca~(2+)/CaM调节的丝氨酸/苏氨酸的蛋白磷酸酶,它广泛分布在脑,心肌,骨骼肌,T淋巴细胞等组织细胞中,通过对底物去磷酸化参与细胞功能的调节。它在T细胞的免疫应答,心肌和骨骼肌的肥厚,神经突触的生长发育及可塑性调节,细胞凋亡等方面都有重要作用。众所周知,在体外循环心脏直视手术时,心脏经历一个缺血再灌注过程,由于缺血再灌注损伤而引起如心律失常,心肌顿抑等心脏功能障碍。目前发生机制主要认为是由于钙超载,氧自由基,能量不足等因素引起。为了进一步研究CaN在心脏中的作用,我们拟在心肌缺血再灌注的前提下,观察CaN的活性的改变,并对其改变的原因作进一步探究。 本实验分两部分: 第一部分:心肌缺血再灌注时CaN活性的测定 目的:建立心肌缺血再灌注模型并检测CaN的活性。 方法:用Wistar大鼠建立Langendorff模型,实验随机分为两组,对照组和实验组(心肌缺血再灌注动物模型,I/R),每组6只大鼠,对照组心脏正常工作30min后灌注30min,实验组心肌正常工作30min后全心缺血30min再灌注30min,心脏正常工作的30min内观察心率,收缩压,以确定心脏在缺血处理前是心脏功能正常的,灌注结束后检测心肌梗死面积,乳酸脱氢酶活性等以确定实验组动物模型的建立,然后两组分别测定CaN活性。 结果:对照组和实验组的动物模型建立的比较成功,两组前30min内,心率均200次/min,收缩压70mmHg,心脏工作正常,实验组梗死面积(32.41±10.04%),对照组并未出现心肌梗死;实验组的乳酸脱氢酶活性(154±10.52U/g)明显高于对照组乳酸脱氢酶活性(7.23±1.25U/g),有统计学意义(P0.05);实验组CaN的活性(0.69±0.13nmolPi/min/μg)低于对照组CaN的活性(0.82±0.15
[Abstract]:Calcineurin can is the only serine / threonine protein phosphatase regulated by Ca ~ (2) / Cam, which is widely distributed in brain, myocardium, skeletal muscle, T lymphocytes and other tissue cells. Dephosphorylation of substrates is involved in the regulation of cell function. It plays an important role in T cell immune response, myocardial and skeletal muscle hypertrophy, synaptic growth and plasticity, apoptosis and so on. It is well known that during open heart surgery under cardiopulmonary bypass, the heart goes through an ischemia-reperfusion process, which results in cardiac dysfunction such as arrhythmia, cardiac arrest and so on. At present, the mechanism is mainly due to calcium overload, oxygen free radicals, energy deficiency and other factors. In order to further study the role of CaN in the heart, we intend to observe the changes of CaN activity under the premise of myocardial ischemia-reperfusion, and to further explore the causes of the changes. This experiment is divided into two parts: part one: determination of CaN activity during myocardial ischemia-reperfusion objective: to establish the heart Muscle ischemia reperfusion model was used to detect the activity of CaN. Methods: the Langendorff model of Wistar rats was established. The rats were randomly divided into two groups: the control group and the experimental group (myocardial ischemia-reperfusion animal model), 6 rats in each group. In the control group, the heart was perfused for 30 minutes after normal operation of 30min, and in the experimental group, the heart rate and systolic blood pressure were observed in the 30min of normal working heart for 30 mins after the normal operation of 30min, so as to determine that the heart function was normal before ischemic treatment. Myocardial infarction area and lactate dehydrogenase activity were measured after perfusion to determine the establishment of experimental animal model. Then CaN activity was measured in both groups. Results: the animal models of the control group and the experimental group were established successfully. The heart rate was 200 beats / min, the systolic pressure was 70 mm Hg, and the infarct area was 32.41 卤10.04% in the control group. No myocardial infarction was found in the control group. The activity of lactate dehydrogenase in the experimental group (154 卤10.52U/g) was significantly higher than that in the control group (7.23 卤1.25U/g) (P0.05), and the activity of CaN in the experimental group (0.69 卤0.13nmolPi/min/ 渭 g) was lower than that in the control group (0.82 卤0.15).
【学位授予单位】：天津医科大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R363

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1 刘宏斌,王思让,李天德,盖鲁粤,杨庭树,智光;急性心肌梗塞面积与心功能的关系[J];中国医学影像学杂志;2000年03期

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