【摘要】：鈣調(diào)神經(jīng)磷酸酶(Calcineurin,CaN)是迄今發(fā)現(xiàn)的唯一受Ca~(2+)/CaM調(diào)節(jié)的絲氨酸/蘇氨酸的蛋白磷酸酶,它廣泛分布在腦,心肌,骨骼肌,T淋巴細(xì)胞等組織細(xì)胞中,通過(guò)對(duì)底物去磷酸化參與細(xì)胞功能的調(diào)節(jié)。它在T細(xì)胞的免疫應(yīng)答,心肌和骨骼肌的肥厚,神經(jīng)突觸的生長(zhǎng)發(fā)育及可塑性調(diào)節(jié),細(xì)胞凋亡等方面都有重要作用。眾所周知,在體外循環(huán)心臟直視手術(shù)時(shí),心臟經(jīng)歷一個(gè)缺血再灌注過(guò)程,由于缺血再灌注損傷而引起如心律失常,心肌頓抑等心臟功能障礙。目前發(fā)生機(jī)制主要認(rèn)為是由于鈣超載,氧自由基,能量不足等因素引起。為了進(jìn)一步研究CaN在心臟中的作用,我們擬在心肌缺血再灌注的前提下,觀察CaN的活性的改變,并對(duì)其改變的原因作進(jìn)一步探究。 本實(shí)驗(yàn)分兩部分: 第一部分:心肌缺血再灌注時(shí)CaN活性的測(cè)定 目的:建立心肌缺血再灌注模型并檢測(cè)CaN的活性。 方法:用Wistar大鼠建立Langendorff模型,實(shí)驗(yàn)隨機(jī)分為兩組,對(duì)照組和實(shí)驗(yàn)組(心肌缺血再灌注動(dòng)物模型,I/R),每組6只大鼠,對(duì)照組心臟正常工作30min后灌注30min,實(shí)驗(yàn)組心肌正常工作30min后全心缺血30min再灌注30min,心臟正常工作的30min內(nèi)觀察心率,收縮壓,以確定心臟在缺血處理前是心臟功能正常的,灌注結(jié)束后檢測(cè)心肌梗死面積,乳酸脫氫酶活性等以確定實(shí)驗(yàn)組動(dòng)物模型的建立,然后兩組分別測(cè)定CaN活性。 結(jié)果:對(duì)照組和實(shí)驗(yàn)組的動(dòng)物模型建立的比較成功,兩組前30min內(nèi),心率均200次/min,收縮壓70mmHg,心臟工作正常,實(shí)驗(yàn)組梗死面積(32.41±10.04%),對(duì)照組并未出現(xiàn)心肌梗死;實(shí)驗(yàn)組的乳酸脫氫酶活性(154±10.52U/g)明顯高于對(duì)照組乳酸脫氫酶活性(7.23±1.25U/g),有統(tǒng)計(jì)學(xué)意義(P0.05);實(shí)驗(yàn)組CaN的活性(0.69±0.13nmolPi/min/μg)低于對(duì)照組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 鹵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 鹵10.52U/g) was significantly higher than that in the control group (7.23 鹵1.25U/g) (P0.05), and the activity of CaN in the experimental group (0.69 鹵0.13nmolPi/min/ 渭 g) was lower than that in the control group (0.82 鹵0.15).
【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

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相關(guān)期刊論文 前1條

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