本文選題：心肌酶 + SOD　； 參考：《吉林大學(xué)》2015年碩士論文

【摘要】：研究背景： 氟乙酰胺是一種高效、劇毒，吸收性強(qiáng)的有機(jī)氟殺鼠劑，殘效期長(zhǎng)，無腐蝕作用。氟乙酰胺中毒起病急，病情發(fā)展迅速，常致心、腦、肺、肝、腎等多臟器損傷。因其可導(dǎo)致人畜的二次中毒，目前已為國(guó)家禁止生產(chǎn)和使用。但因其效果明顯，許多商販仍進(jìn)行違法生產(chǎn)及出售，使得氟乙酰胺中毒事件時(shí)有發(fā)生，近年甚至有上升趨勢(shì)。氟乙酰胺對(duì)心臟有明顯損害，，體現(xiàn)在對(duì)心肌細(xì)胞及傳導(dǎo)系統(tǒng)的損害，心肌損害率80%以上，可致各種心律失常，心功能衰竭，血壓下降，甚至心室顫動(dòng)，心功能異常是其第二位死亡原因。目前公認(rèn)的中毒機(jī)制為氟乙酰胺使三羧酸循環(huán)中斷，從而導(dǎo)致各臟器損傷，對(duì)中毒后心肌損傷的情況及治療缺乏進(jìn)一步研究。探討氟乙酰胺中毒引起心肌損傷的情況及有效的治療方法，對(duì)降低死亡率、改善預(yù)后有重要意義。 目的： 探討大鼠氟乙酰胺中毒后心肌損傷情況，與氧化損傷的關(guān)系；乙酰胺聯(lián)合前列地爾注射液對(duì)中毒大鼠心肌損傷是否具有保護(hù)作用。 方法： 通過灌胃方法制作氟乙酰胺中毒大鼠模型，共100只大鼠，雌雄各半，將其隨機(jī)分成5組。A組為正常對(duì)照組，1ml生理鹽水灌胃，并每日給予等劑量生理鹽水腹腔注射。B組為氟乙酰胺染毒組，氟乙酰胺溶液按6mg/kg灌胃制作氟乙酰胺中毒模型，并每日給予等劑量生理鹽水腹腔注射。C組為乙酰胺治療組，氟乙酰胺溶液按6mg/kg灌胃制作氟乙酰胺中毒模型，染毒后1小時(shí)按2.8g/kg給予乙酰胺，日二次（Q12H）腹腔注射。D組為乙酰胺+前列地爾注射液治療組，氟乙酰胺溶液按6mg/kg灌胃制作氟乙酰胺中毒模型，染毒后1小時(shí)按2.8g/kg給予乙酰胺，日二次（Q12H）腹腔注射，同時(shí)按10ug/kg加用前列地爾注射液，日一次腹腔注射。E組為前列地爾注射液治療組，氟乙酰胺溶液按6mg/kg灌胃制作氟乙酰胺中毒模型，染毒后1小時(shí)按前列地爾注射液10ug/kg QD腹腔注射。在5組大鼠染毒后不同時(shí)間點(diǎn)（4h、1d、3d、7d）取心肌組織行HE染色觀察心肌形態(tài)變化；測(cè)定血液中磷酸肌酸激酶（CK）、磷酸肌酸同工酶（CK-MB）、天門冬氨酸氨基轉(zhuǎn)移酶（AST）及心肌組織中超氧化物歧化酶（SOD）、丙二醛（MDA）的含量，行統(tǒng)計(jì)學(xué)分析，探討其意義。 結(jié)果： HE染色提示氟乙酰胺中毒大鼠心肌損傷于1d開始出現(xiàn)，呈點(diǎn)狀或局灶性變性、壞死，其周圍細(xì)胞胞漿染色嗜酸性增強(qiáng)，伴少量炎細(xì)胞浸潤(rùn)；3d損傷最重，心肌細(xì)胞大片狀壞死、溶解消失，大量炎細(xì)胞浸潤(rùn)；D組與C組7d開始出現(xiàn)肉芽組織；D組與C組、E組相比較，心肌損傷范圍小，程度輕。心肌三酶4h開始升高，1d達(dá)到高峰，3d下降，7d基本恢復(fù)正常。D組1d時(shí)AST及CK-MB值與B組、E組相比具有統(tǒng)計(jì)學(xué)意義（P＜0.01），其余時(shí)間點(diǎn)D組心肌三酶與C組、E組相比無明顯差異（P＞0.05）。氟乙酰胺中毒后心肌SOD含量降低、MDA含量升高，與對(duì)照組相比有顯著差異（P＜0.01）；D組與C組、E組心肌MDA含量相比明顯降低（P＜0.01）；SOD含量三組之間相比無統(tǒng)計(jì)學(xué)意義（P＞0.05）。 結(jié)論： （1）氟乙酰胺中毒可導(dǎo)致心肌損傷，主要表現(xiàn)為心肌局灶性或片狀壞死，伴有炎細(xì)胞浸潤(rùn)。在中毒后3d損傷最重。心肌酶1d達(dá)到高峰，7d基本恢復(fù)正常。 （2）健康大鼠氟乙酰胺中毒后心肌組織中SOD含量減少，MDA含量增加，考慮心肌損傷與氧化損傷有關(guān)。 （3）乙酰胺聯(lián)合前列地爾注射液對(duì)大鼠氟乙酰胺中毒所致心肌損傷具有保護(hù)作用，與乙酰胺治療組及前列地爾治療組相比，可明顯減輕心肌損傷范圍及程度；縮短心肌組織修復(fù)時(shí)間;能清除氧自由基，有效降低心肌組織MDA含量，達(dá)到抗氧化損傷作用。
[Abstract]:Research background:
Fluoro acetamide is a highly effective, highly toxic and Absorbable Organic Fluorine killer, which has long residual effect and no corrosion effect. Fluoro acetamide poisoning is urgent and develops rapidly. It often causes multiple organ damage in heart, brain, lung, liver and kidney. Because it can lead to two poisoning of human and animal, it has been banned from production and use in the country. The drug traffickers still carry out illegal production and sale, making the fluoro acetamide poisoning happen and even rising in recent years. The fluoro acetamide has obvious damage to the heart, which is reflected in the damage to the cardiac myocytes and conduction system, the rate of myocardial damage is above 80%, and can cause various arrhythmia, heart failure, blood pressure drop, even ventricular fibrillation, cardiac function Abnormality is the second cause of death. The current recognized mechanism of poisoning is that fluoro acetamide interrupts the circulation of three carboxylic acids, which leads to the injury of various organs, and the lack of further study on the condition of myocardial injury after poisoning and the treatment of myocardial injury caused by fluoro acetamide poisoning, and to reduce the mortality and improve the precondition. It is of great significance.
Objective:
To investigate the relationship between myocardial injury and oxidative damage in rats after fluoroacetamide poisoning, and whether acetamide and Alprostadil Injection have protective effect on myocardial injury in rats.
Method:
A rat model of fluoro acetamide poisoning was made by gavage. A total of 100 rats were divided into 5 groups of.A groups. The rats were divided into 5 groups as normal control group, 1ml saline was given to the stomach, and.B group was given daily dose of saline as the fluoro acetamide group. The fluoro acetamide solution was injected into the stomach to make the fluoro acetamide poisoning model. A daily dose of normal saline was given to the group of.C in the group of acetamide. Fluoroacetamide was injected into the stomach to make a model of fluoroacetamide poisoning according to 6mg/kg. 1 hours after exposure to 2.8g/kg was given to acetamide. Two times (Q12H) was injected into the.D group as the acetamide + Alprostadil Injection treatment group. Fluoroacetamide solution was made by 6mg/kg to make fluorine and B. The model of amidotoxism was given to acetamide by 2.8g/kg 1 hours after exposure, two times (Q12H) intraperitoneal injection, and 10ug/kg added to Alprostadil Injection,.E group was injected into group.E once daily, and fluoroacetamide solution was injected by 6mg/kg to produce fluoroacetamide poisoning model, and 1 hours after exposure to Alprostadil Injection 10. Ug/kg QD was intraperitoneally injected. Myocardial morphologic changes were observed at different time points (4h, 1D, 3D, 7D) at different time points (4h, 1D, 3D, 7D); the content of creatine phosphate kinase (CK), creatine phosphate isozyme (CK-MB), aspartate aminotransferase (AST) and the content of MDA (MDA) in myocardial tissue were measured. Statistical analysis was used to discuss its significance.
Result:
HE staining suggested that myocardium injury in rats with fluoroacetamide poisoning began to appear in 1D, showing spot or focal degeneration, necrosis, cytosolic staining of eosinophilic cells and infiltration of a small amount of inflammatory cells in the surrounding cells; 3D injury was the heaviest, myocardial cells were necrotic, dissolution disappeared, and large number of inflammatory cells infiltrated; group D and C group 7d began to appear granulation tissue; D group; D group. Compared with group C and group E, the range of myocardial injury was small and the degree of myocardial three enzyme 4H began to rise, 1D reached its peak, 3D decreased. When 7d basically recovered the 1D of normal.D group, the value of AST and CK-MB was statistically significant compared with the E group. The remaining time points had no significant difference between the three enzymes and the group (0.05). The content of muscle SOD decreased and the content of MDA increased significantly (P < 0.01) compared with the control group (P < 0.01). The myocardial MDA content in group D and C group was significantly lower than that in group E (P < 0.01), and there was no significant difference between the three groups of SOD (P > 0.05).
Conclusion:
(1) fluoroacetamide poisoning can cause myocardial injury, mainly manifested as focal or flaky necrosis of the myocardium with inflammatory cell infiltration. After poisoning, the 3D damage is the heaviest. The myocardial enzyme 1D reaches the peak, and the 7d is basically restored to normal.
(2) in healthy rats, SOD content in myocardium decreased and MDA content increased after fluoramide poisoning.
(3) acetamide combined with Alprostadil Injection has protective effect on myocardial injury caused by fluoroacetamide poisoning in rats. Compared with acetamide group and alprostadil treatment group, it can obviously reduce the extent and degree of myocardial injury, shorten the time of myocardial repair, scavenge oxygen free radicals, reduce the MDA content of myocardial tissue, and achieve oxygen resistance. Chemical damage.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R595.4

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 廖信彪;余彥耿;周健;;氟乙酰胺中毒死亡的法醫(yī)病理學(xué)分析報(bào)告[J];廣東公安科技;2014年04期

2 聶國(guó)明,楊新鳳;48例氟乙酰胺中毒臨床分析及納洛酮療效觀察[J];華南國(guó)防醫(yī)學(xué)雜志;2001年01期

3 吳秀明,戴建偉;氟乙酰胺中毒患者血清酶及心電圖測(cè)定的臨床意義[J];醫(yī)學(xué)臨床研究;2004年08期

4 曾能初;氟乙酰胺中毒心電圖改變54例分析[J];井岡山醫(yī)專學(xué)報(bào);2002年03期

5 劉仁樹,吳天明,王洪宗;46例急性氟乙酰胺中毒致死者的臨床特征回顧與啟迪[J];急診醫(yī)學(xué);1997年04期

6 吳偉鴻,李翠瓊;急性氟乙酰胺中毒11例臨床分析[J];勞動(dòng)醫(yī)學(xué);2000年03期

7 熊錦,徐孝玄,周紅珍,魯祖建;急性氟乙酰胺中毒致QTc離散度改變的意義[J];中原醫(yī)刊;2001年05期

8 楊凌飛,周志明,陳愛華;急性氟乙酰胺中毒致心肌損害35例臨床分析[J];內(nèi)科急危重癥雜志;2000年04期

9 吳連春;;前列地爾的臨床應(yīng)用進(jìn)展[J];河北聯(lián)合大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2013年02期

10 馬龍;畢玉磊;邱麗麗;胡英華;;炎性細(xì)胞因子對(duì)中毒性心肌損害的診斷價(jià)值[J];大家健康(學(xué)術(shù)版);2014年12期

本文編號(hào)：2109415