【摘要】：目的觀察去腎交感神經(jīng)術(shù)(RDN)治療犬心肌梗死(簡稱心梗)的效果,并探討其相關(guān)機(jī)制。方法 18只健康雜種犬隨機(jī)分為對照組、模型組、治療組,每組6只。模型組、治療組采用明膠海綿栓塞法建立前壁心梗模型;造模后1周,治療組行RDN手術(shù),模型組只行腎動脈造影檢查。分別于造前及造模后4周檢測左心室射血分?jǐn)?shù)(LVEF)、短軸縮短率(FS)、左心室舒張末期壓(LVEDP)、左心室收縮末期壓(LVSP)及心率(HR)。造模后4周采用苦味酸比色法測定血肌酐。建模后4周處死動物,留取梗死周邊區(qū)組織(對照組取同一部位組織),HE染色觀察心肌形態(tài)及結(jié)構(gòu)改變;同時檢測心肌組織AngⅡ、Ang1-7、ACE2 mRNA、MasR mRNA。建模后4周,留取實(shí)驗(yàn)犬腎動脈組織,采用免疫組化染色觀察腎動脈酪氨酸羥化酶(TH)陽性神經(jīng)纖維形態(tài)及分布情況并進(jìn)行定量分析。結(jié)果模型組和治療組造模后4周LVEDP高于對照組,LVEF、FS、LVSP低于對照組(P均0.05);治療組LVEDP低于模型組,LVEF高于模型組(P均0.05)。對照組、模型組和治療組血肌酐水平相比,P均0.05。治療組較模型組梗死周邊區(qū)病理改變明顯減輕。模型組和治療組心肌組織中AngⅡ、Ang1-7水平及ACE2 mRNA、MasR mRNA相對表達(dá)量高于對照組,治療組AngⅡ、Ang1-7水平及ACE2 mRNA、MasR mRNA相對表達(dá)量低于模型組(P均0.05)。治療組與模型組相比,TH陽性神經(jīng)纖維形態(tài)及分布趨于正常,且治療組TH陽性神經(jīng)纖維相對表達(dá)量低于模型組(P0.05)。結(jié)論 RDN治療犬心梗有效,可改善心功能,減輕心肌病理改變,作用可能與AngⅡ、Ang1-7、ACE2、MasR水平下調(diào)及ACE-AngⅡ-AT1R軸與ACE2-Ang1-7-MasR軸功能失衡改善有關(guān)。
[Abstract]:Objective to observe the effect of (RDN) in the treatment of canine myocardial infarction (MI) and to explore its related mechanism. Methods 18 healthy mongrel dogs were randomly divided into control group, model group and treatment group with 6 dogs in each group. Model group, the treatment group was embolized with gelatin sponge to establish the model of anterior myocardial infarction, 1 week after the model, the treatment group underwent RDN operation, and the model group only underwent renal arteriography. Left ventricular ejection fraction (LVEF),) short axis shortening rate (LEF) (FS), left ventricular end-diastolic pressure (FS),) (LVEDP), left ventricular end-systolic pressure (LVSP) and heart rate (HR). Were measured before and 4 weeks after modeling. Serum creatinine was determined by picric acid colorimetry 4 weeks after modeling. The animals were killed 4 weeks after modeling, and the myocardial morphology and structure were observed by HE staining and Ang 鈪，

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