兔心脏淋巴循环阻滞后Ⅰ、Ⅲ型胶原蛋白变化的实验研究

发布时间：2018-04-12 07:47

  本文选题：兔 + 心脏淋巴　； 参考：《泰山医学院》2005年硕士论文

【摘要】：目的早在上世纪60年代国外许多学者就对心脏淋巴的解剖生理及病理做了大量研究,1963年Miller等把狗的心脏淋巴阻滞后通过观察提出心脏淋巴循环障碍是心内膜纤维化的重要机制。近些年来有学者提出心脏淋巴循环障碍与冠脉、心肌间质纤维化存在着一定联系。有学者阻滞山羊心脏淋巴后对冠状动脉结构作了急性期和慢性期的观察,发现阻滞淋巴10-14天,冠状动脉和小动脉内膜内皮肿胀,排列紊乱,中膜水肿,浅层和外膜纤维结缔组织增生。60-180天动脉内膜中膜水肿明显减轻,但外膜和心肌间质仍有纤维结缔组织增生。结缔组织增生是因为组织中未能通过淋巴回流的高浓度的蛋白刺激纤维母细胞增生所致。本研究通过观察兔心脏淋巴循环阻滞后血清中Ⅰ型前胶原羧基端肽(PICP)、Ⅲ型前胶原氨基端肽(PIIINP)和血管紧张素Ⅱ(AngⅡ)的变化规律,并用原位杂交的方法测定不同观察时间点心肌间质Ⅰ、Ⅲ型胶原蛋白mRNA的表达,探讨心脏淋巴循环阻滞后心肌间质纤维化的机制。 方法将34只健康成年新西兰白兔随机分为实验组和对照组,每组各半。用3%戊巴比妥钠(30mg/kg)静脉麻醉后,行气管插管,连接小动物呼吸机,进行辅助呼吸,心电监护,沿胸骨正中切口,切开胸骨,打开心包暴露心脏,分别于左右心室靠近心尖部注射10%亚甲兰0.5ml,可见心外膜下向心底回流的淋巴干,沿淋巴干走行的方向分别将主动脉与肺动脉间和主动脉后方与右肺上动脉间的淋巴结群灼烧,结扎其远端淋巴管,逐层关闭胸腔。对照组除不结扎淋巴管、灼烧淋巴结外其余同实验组。分别于术前、术后3、7、14、30、60d取静脉血,应用ELISA法测定血清中PICP、PIIINP和AngⅡ的浓度；用原位杂交的方法测定各个观察点Ⅰ、Ⅲ型胶原蛋白mRNA的表达。 结果实验组AngⅡ与PICP、PIIINP在结扎兔心脏淋巴循环后3和60天与结扎前差异无显著性,与相应对照组无显著性差异(P0.05)；结扎后7、14和30天明显高于术前且明显高于相应对照组(P0.05)；对照组术前与术后无显著性差异(P0.05)。PICP、PIIINP与AngⅡ有高度相关性(P0.05)。实验组原位杂交实验结果表明Ⅱ、Ⅲ型胶原蛋白mRNA的表达与血清中PICP、PIIINP的变化一致。 结论兔心脏淋巴循环阻滞后,心肌间质中Ⅰ、Ⅲ型胶原蛋白于第7d开始合成增加,持续至30d,60d恢复正常。Ⅰ、Ⅲ型胶原蛋白增加是心脏淋巴循环阻滞后心肌间质纤维化的原因之一
[Abstract]:Objective as early as the 1960s, many foreign scholars have done a lot of research on the anatomy, physiology and pathology of cardiac lymph nodes. In 1963, Miller et al showed that the dysfunction of cardiac lymphatic circulation was an important mechanism of endocardial fibrosis after cardiac lymphoid block in dogs.In recent years, some scholars have suggested that cardiac lymphatic circulatory disorder is related to coronary artery and myocardial interstitial fibrosis.Some scholars observed the structure of coronary artery in acute and chronic phase after blocking cardiac lymph nodes in goats. It was found that the endothelium of coronary artery and arteriole intima was swollen, disordered, and middle membrane edema was observed after 10 ~ 14 days of lymphatic block.Superficial and adventitia fibrous connective tissue proliferation. 60-180 days of arterial intima media edema significantly reduced, but there is still fibrous connective tissue proliferation in adventitia and myocardial stroma.Connective tissue hyperplasia is caused by the high concentration of protein in the tissue that fails to flow through lymphatic reflux to stimulate fibroblast proliferation.In this study, we observed the changes of procollagen type I carboxyl terminal peptide (PICPN), type 鈪，

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