本文選題：法舒地爾 + 阿霉素　； 參考：《廣西醫(yī)科大學(xué)》2014年碩士論文

【摘要】：目的：研究法舒地爾（Fas）干預(yù)對(duì)阿霉素（ADM）致大鼠血清肌鈣蛋白（cTnI）、ATP、ADP、光鏡及電鏡超微結(jié)構(gòu)的變化和影響，從而探討Fas干預(yù)對(duì)ADM誘導(dǎo)心肌損傷的保護(hù)作用，為癌癥患者的圍術(shù)期心肌保護(hù)提供一定的實(shí)驗(yàn)依據(jù)。 方法：將體重200g左右的32只雌性大鼠隨機(jī)分成4組，每組8只。（1）A組（空白對(duì)照）：于實(shí)驗(yàn)第1、3、5、7、9、11天（9：00AM）腹腔注射生理鹽水，每次10ml/kg；第14天開(kāi)始，每次10ml/kg/天，連續(xù)6天。（2）B組（ADM+生理鹽水）：于實(shí)驗(yàn)第1、3、5、7、9、11天（9：00AM）腹腔注射ADM2.5mg/kg；第14天起，每日生理鹽水10ml/kg/次，連續(xù)6天。（3）C組（ADM+Fas10mg/kg/天）：前6次給藥同B組，于實(shí)驗(yàn)第14天起注射Fas，每次10mg/kg/天，連續(xù)6天。（4）D組（ADM+Fas2mg/kg/天）：前6次給藥同B組，于實(shí)驗(yàn)第14天起注射Fas，每次2mg/kg/天，連續(xù)6天。在最后一次給藥后第4天，腹腔注射10%的水合氯醛麻醉大鼠。分別在實(shí)驗(yàn)開(kāi)始前（T1）、注射ADM48小時(shí)后（T2）、注射Fas24小時(shí)后（T3）、麻醉后（T4）四個(gè)時(shí)間點(diǎn)采血，檢測(cè)血清cTnI水平；檢測(cè)4組小鼠心肌ATP、ADP含量。留取心肌組織觀察光鏡、電鏡下的病理變化。 結(jié)果：(1)在T2時(shí)點(diǎn)，B、C、D三組大鼠的cTnI值與A組相比均顯著升高（P0.01），而B(niǎo)、C、D三組之間無(wú)顯著差異（P0.05）；在T3時(shí)點(diǎn)，C、D兩組與B組的cTnI值比較有明顯下降（P0.01)，而C、D兩組間也存在顯著差異（P0.01）；在T4時(shí)點(diǎn)C、D兩組與B組的cTnI值比較同樣有明顯下降（P0.01)，但C、D兩組間無(wú)明顯差異（P0.05）；C、D兩組在T2時(shí)點(diǎn)cTnI水平最高；而C組在T3、T4時(shí)點(diǎn)中的cTnI值有統(tǒng)計(jì)學(xué)意義（P0.05）；D組在T3、T4時(shí)點(diǎn)中的cTnI值無(wú)統(tǒng)計(jì)學(xué)差異（P0.05）。（2）四組大鼠的ADP值比較均有統(tǒng)計(jì)學(xué)差異（P0.05）；而C、D兩組間的ATP值比較無(wú)統(tǒng)計(jì)學(xué)差異（P0.05），其余各組間的比較有顯著差異（P0.05）。（3）大鼠的心肌損傷病理評(píng)分，B、C、D組與A組相比均升高（P0.01）；但與B組相比，干預(yù)后的C、D兩組明顯有所改善，，評(píng)分較低（P0.05）；C、D間無(wú)顯著差異（P0.05）。（4）心肌電鏡超微結(jié)構(gòu)，除A組表現(xiàn)正常，其余三組均發(fā)生嚴(yán)重改變，其中B組損傷表現(xiàn)最為嚴(yán)重，C組優(yōu)于D組，但仍然不及A組超微結(jié)構(gòu)正常、清晰。 結(jié)論：（1）ADM導(dǎo)致大鼠心肌損傷，血清cTnI水平顯著上升，心肌ADP、ATP含量明顯下降；（2）Fas干預(yù)ADM誘導(dǎo)后的大鼠，血清cTnI水平下降，心肌ATP、ADP含量明顯升高，病理評(píng)分明顯下降，心肌超微結(jié)構(gòu)得到改善，提示Fas對(duì)ADM誘導(dǎo)的心肌損傷有一定的保護(hù)作用。
[Abstract]:Objective: to study the changes and effects of fascia on the changes and ultrastructure of troponin cTnInAP-ATPase in serum of rats induced by adriamycin (ADM), so as to explore the protective effect of Fas intervention on myocardial injury induced by ADM. To provide a certain experimental basis for perioperative myocardial protection of cancer patients. Methods: Thirty-two female rats weighing about 200g were randomly divided into 4 groups, 8 rats in each group, 8 rats in each group (control group: 9: 00 amm, 911 days after experiment), 10 ml / kg of normal saline was injected intraperitoneally, and 14 days later, every 10ml/kg/ day. In group B, adm 2.5 mg / kg was injected intraperitoneally on the 1st day of the experiment, followed by intraperitoneal injection of ADM 2.5 mg / kg on the 14th day. Daily normal saline 10ml/kg/ was given daily for 6 days. Group C was given the same drug as group B on the 14th day of the experiment. Group D was given Fas2mg/kg/ for 6 consecutive days: the first 6 times were given to the same group as group B, and 2mg/kg/ was injected on the 14th day of the experiment for 6 days, each time for 6 days. On the fourth day after the last administration, 10% chloral hydrate was injected intraperitoneally to anesthetized rats. The blood samples were collected at four time points before the beginning of the experiment, after ADM48 injection, after injection of Fas24, and after anesthesia, respectively. The levels of serum cTnI and the content of Fas24 in myocardium of the four groups were detected. Myocardial tissue was taken to observe the pathological changes under light microscope and electron microscope. Results at T2, the cTnI values of the three groups were significantly higher than those of the group A, but there was no significant difference among the three groups. The cTnI value of the two groups was significantly lower than that of the group B at T3 time, and there was a significant difference between the two groups, and there was also a significant difference between the two groups. At T4, the cTnI values of group C and group B also decreased significantly, but there was no significant difference between group C and group D in cTnI level at T 2, but there was no significant difference between group D and group C (P 0.05) at T _ 2 time, but the level of cTnI was the highest in group C _ (0.05) and C _ (D) at T _ 2. There was no significant difference in cTnI value between group C and group D at T3 / T4. (P < 0.05) the ADP value of group C was significantly different from that of group C (P < 0.05), but there was no significant difference in ATP value between the two groups (P0.05), while the other two groups had no significant difference in ATP value between the two groups (P0.05), while the ADP value of group C had no statistical difference in T3 / T4 time (P < 0.05); the ADP value of group C was significantly different from that of group C (P < 0.05); and there was no significant difference in ATP value between the two groups. The pathological score of myocardial injury was significantly higher in group B than in group A, but it was higher in group B than in group B, but it was significantly higher in group B than in group B, but it was significantly higher in group B than in group B, but it was significantly higher in group B than that in group A, but it was higher in group B than in group B. There was no significant difference between the two groups after intervention. The ultrastructure of myocardium in group A was normal, and the other three groups had serious changes. Group B had the most severe injury than group D. The group C had the most serious injury than the group D, and the ultrastructure of myocardium in group C was better than that in group D. the ultrastructure of myocardium in group C was more serious than that in group D, except for group A, which was normal and the other three groups had serious changes. However, the ultrastructure of group A was still not normal and clear. Conclusion the level of cTnI in serum of rats induced by cTnI was significantly increased, and the level of cTnI in serum decreased, and the pathological score was significantly decreased in rats after ADM was induced by Fas. Myocardial ultrastructure was improved, suggesting that Fas has a protective effect on myocardial injury induced by ADM.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R614

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 段紀(jì)俊;陳萬(wàn)青;張思維;;中國(guó)惡性腫瘤死亡率的國(guó)際比較[J];中國(guó)社會(huì)醫(yī)學(xué)雜志;2009年06期

2 師幸偉;程冕;白融;阮磊;閆杰;侯宏偉;李秀琪;宋玉娥;;阿霉素誘導(dǎo)兔心衰模型的建立與評(píng)價(jià)[J];動(dòng)物醫(yī)學(xué)進(jìn)展;2013年03期

3 薛成愛(ài);劉永芹;;鹽酸法舒地爾對(duì)急性心肌梗死患者的療效觀察[J];河北醫(yī)藥;2011年04期

4 花冠杰;韋利元;韋穎;;鹽酸法舒地爾對(duì)冠心病心力衰竭的臨床療效觀察[J];檢驗(yàn)醫(yī)學(xué)與臨床;2011年10期

5 馬建英;譚麗娟;潘娜娜;;法舒地爾對(duì)急性心肌梗死大鼠炎性細(xì)胞因子表達(dá)的影響[J];臨床心血管病雜志;2011年04期

6 王新;錦見(jiàn)俊雄;;法舒地爾對(duì)鹽敏感大鼠腎小球硬化癥的弱化作用[J];臨床心血管病雜志;2011年09期

7 莊艷;劉先領(lǐng);;蒽環(huán)類(lèi)藥物心臟毒性及其預(yù)防措施[J];腫瘤藥學(xué);2011年04期

8 石偉利;;鹽酸法舒地爾對(duì)冠心病心力衰竭患者心室重構(gòu)和心功能的影響[J];內(nèi)蒙古醫(yī)學(xué)雜志;2010年02期

9 倪敏霞;武曉云;楊華;楊迎蘭;;Rho激酶抑制劑法舒地爾治療COPD合并肺動(dòng)脈高壓的療效觀察[J];寧夏醫(yī)學(xué)雜志;2010年12期

10 蔣智慧;張俊峰;龍盼;張?zhí)锾?;鹽酸法舒地爾后適應(yīng)對(duì)大鼠心肌缺血再灌注損傷的保護(hù)作用[J];中華老年心腦血管病雜志;2012年05期

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