本文關(guān)鍵詞： 慢性腎功能衰竭 腎透析 微炎癥 慢性心力衰竭 超聲心動(dòng)描記術(shù)　出處：《石河子大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:研制慢性腎功能衰竭(CKD)微炎癥狀態(tài)下心力衰竭大鼠模型并探索其心衰機(jī)制。方法:SD大鼠70只,隨機(jī)分為3組:對照組(10只)食用油10ml·kg-1·d-1灌胃,1次/d;CKD組(30只)3%腺嘌呤食用油10ml·kg-1·d-1灌胃;造模組(30只)初始腺嘌呤灌胃同CKD組,Scr升高1.5倍腺嘌呤灌胃減為1次/3d,開始腹腔注射阿霉素2.5mg/kg,1次/7d,10 mg/L溴酸鉀溶液代替飲水。監(jiān)測腎功、C-反應(yīng)蛋白及心臟超聲。造模成功后對比各組心臟超聲、全心質(zhì)量指數(shù)(HM/BM)及左心室質(zhì)量指數(shù)(LVM/BM)、病理學(xué)特點(diǎn)。對比各組基質(zhì)金屬蛋白酶-2、9(MMP-2、9)及基質(zhì)金屬蛋白酶抑制劑-1(TIMP-1),VG染色病理學(xué)及膠原面積百分比,電鏡超微結(jié)構(gòu)及心肌細(xì)胞的凋亡。結(jié)果:(1)模型達(dá)標(biāo)情況:從CKD、心力衰竭和微炎性反應(yīng)評價(jià),造模達(dá)標(biāo)。(2)心臟超聲:造模組左心室舒張末期內(nèi)徑(LVEDd)、左心室收縮末期內(nèi)徑(LVESd)、左心室舒張末期容積(LVEDV)、左心室收縮末期容積(LVESV)升高,收縮末期室間隔厚度(IVSs)、左心室收縮末期后壁厚度(LVPWs)降低,縮短分?jǐn)?shù)(FS)、左室射血分?jǐn)?shù)(LVEF)下降,與對照組及CKD組有統(tǒng)計(jì)學(xué)差異(P均0.05);CKD組與對照組相比LVESd、LVESV升高,FS、LVEF下降(P均0.05)。(3)HM/BM及LVM/BM:與對照組相比,CKD組及造模組增高(P均0.05),但兩組間無統(tǒng)計(jì)學(xué)差異。(4)病理學(xué):HE染色造模組心肌細(xì)胞及纖維破壞伴單核細(xì)胞浸潤;CKD組病變較輕且不伴炎細(xì)胞浸潤。VG染色及電鏡超微結(jié)構(gòu)中,CKD組及造模組心肌病理損傷逐漸加重,VG染色各組膠原面積與所測視野的面積比分別為0.132、0.151、0.053。(5)金屬蛋白酶測定:MMP-2,造模組低于對照組及CKD組;CKD組低于對照組,差異接近但尚未達(dá)統(tǒng)計(jì)學(xué)標(biāo)準(zhǔn)(P=0.058)。MMP-9和TIMP-1,各組間無統(tǒng)計(jì)學(xué)差異,但其比值隨著心衰程度的逐漸加重而顯著升高,除CKD組與造模組差異接近但尚未達(dá)統(tǒng)計(jì)學(xué)標(biāo)準(zhǔn)外(P=0.055),其他均有統(tǒng)計(jì)學(xué)意義。(6)細(xì)胞凋亡測定:未見心肌細(xì)胞凋亡。結(jié)論:(1)腺嘌呤灌胃聯(lián)合阿霉素腹腔注射,溴酸鉀溶液飲水可建立慢性腎功能衰竭微炎癥狀態(tài)下心力衰竭大鼠模型。(2)慢性腎功能衰竭微炎癥狀態(tài)下大鼠心力衰竭的機(jī)制是心功能下降、心臟相對增重及相應(yīng)的心肌病理損害,并出現(xiàn)心肌細(xì)胞外基質(zhì)減少,心室重構(gòu)明顯,但尚未出現(xiàn)心肌細(xì)胞凋亡。(3)除心臟相對增重外,單純CKD上述其他表現(xiàn)均明顯輕于慢性腎功能衰竭微炎癥狀態(tài)下心力衰竭。
[Abstract]:Objective: to develop a rat model of heart failure induced by chronic renal failure (CKD) microinflammation and to explore the mechanism of heart failure. The rats were randomly divided into three groups: control group (n = 10): 10 ml 路kg-1 路d ~ (-1) of edible oil (n = 30) were perfused with 10 ml 路kg-1 路d ~ (-1) of 3% adenine. 30 rats in the model group) the initial adenine administration was 1. 5 times higher than that in the CKD group. Adenine administration was reduced to 1 / 3 d, and was injected intraperitoneally with doxorubicin 2.5 mg / kg / 1 / 7 d / 10 mg/L potassium bromate solution instead of drinking water. Renal function C-reactive protein (CRP) and cardiac ultrasound were monitored. After the model was successful, the echocardiography of each group was compared. Total cardiac mass index (HM / BMN) and left ventricular mass index (LVM / BMN), histopathological characteristics, pathological characteristics, and matrix metalloproteinase inhibitor (MMP-2) and matrix metalloproteinase inhibitor (TIMP-1 / VG) staining were compared in each group. Ultrastructure of electron microscope and apoptosis of cardiomyocytes. Results: CKD, heart failure and microinflammatory response were evaluated from CKD, heart failure and microinflammatory response. Cardiac ultrasound: left ventricular end-diastolic diameter (LVED), left ventricular end-systolic diameter (LVES), left ventricular end-diastolic volume (LVEDVV), left ventricular end-systolic volume (LVESVV) were increased in model group. The left ventricular posterior wall thickness (LVPWs) decreased, the left ventricular ejection fraction (LVEF) decreased, the left ventricular ejection fraction (LVEF) decreased, the left ventricular septal thickness decreased, the left ventricular posterior wall thickness (LVPWs) decreased, and the left ventricular ejection fraction (LVEF) decreased. There was significant difference between CKD group and control group (P < 0.05). Compared with control group, LVESdsLVESV increased and LVEF decreased (P < 0.05). HM-BM and LVM-BM: compared with control group, CKD group and model group were 0.05p, but there was no statistical difference between two groups. Myocardial cell and fiber destruction with monocyte infiltration in CKD group with mild lesion and no inflammatory cell infiltration. VG staining and ultrastructural changes of cardiomyopathy in CKD group and model group were gradually aggravated. The area ratio of visual field to visual field was 0.132 / 0.151 / 0.053.5) the ratio of metalloproteinases to MMP-2 in the model group was lower than that in the control group and the CKD group was lower than that in the control group, and that in the CKD group was lower than that in the control group. The difference was close but not up to the statistical standard. There was no statistical difference among the three groups, but the ratio increased with the increase of heart failure. Except that the difference between CKD group and model group was similar but not up to the statistical standard, there was no myocardial apoptosis. Conclusion: 1) adenine plus adriamycin was injected intraperitoneally. Potassium bromate solution can establish a rat model of chronic renal failure induced by microinflammation) the mechanism of heart failure in rats with microinflammation of chronic renal failure is the decrease of cardiac function. The relative weight gain of the heart and the corresponding pathological damage of cardiomyopathy resulted in the decrease of extracellular matrix and ventricular remodeling, but no cardiomyocyte apoptosis was found, except for the relative weight gain of the heart. All the other findings mentioned above in CKD alone were significantly less than those in chronic renal failure with microinflammation.
【學(xué)位授予單位】：石河子大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R692.5;R541.6;R-332

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