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目的探讨甲状腺素诱导的心脏病大鼠左室心肌重构和血浆脑钠素水平的变化,并采用药物缬沙坦进行干预,观察缬沙坦对甲亢性心脏病大鼠的心脏保护作用。方法Sprage-Dawley(SD)大鼠40只,按随机分组原则分为对照组、L-甲状腺素组、缬沙坦小剂量组(L-甲状腺素+10 mg/kg缬沙坦)、缬沙坦大剂量组(L-甲状腺素+30 mg/kg缬沙坦)。甲状腺素组和缬沙坦干预组予L-甲状腺素0.5 mg/(kg.d)腹腔注射28 d建立甲亢模型,缬沙坦小剂量组在建模同时予缬沙坦10 mg/(kg.d)灌胃治疗,缬沙坦大剂量组灌服缬沙坦30 mg/(kg.d)。造模前后分别采取静脉血,用化学发光法检测血清T3、T4水平;酶联免疫法测血浆脑钠素(brain natriuretic peptide,BNP)水平;第28天行超声心动图检测左室舒张末期内径(LVDD)、左室后壁(LVPW)、室间隔(IVS)厚度。完成心脏超声检查后解剖动物测定各组大鼠心肌肥厚指数;收集左室心肌组织分别行HE染色和Masson染色观察左心室心肌组织形态结构、测定左心室细胞直径和胶原容积分数(collagen volume fraction,CVF)。结果L-甲状腺素腹腔注射4周可成功制备甲亢性心脏病模型,与对照组相比,L-甲状腺素组大鼠左室腔扩大,室壁增厚,心指数、心肌细胞直径、胶原容积分数增大;BNP水平:L-甲状腺素组血浆(776.61±193.99)pg/mL明显高于对照组(47.11±23.19)pg/mL(P<0.01),而缬沙坦大剂量(340.16±139.55)pg/mL、小剂量组(371.64±164.49)pg/mL水平均较未干预组明显减低(P<0.01),缬沙坦大、小剂量干预组大鼠之间以上指标差异无统计学意义。结论甲状腺素可诱导大鼠左室心肌细胞肥大,基质纤维组织增生,心室腔扩大及血浆BNP水平升高。缬沙坦具有抑制其心肌重构,降低血浆BNP水平的作用,血浆BNP水平可能为早期诊断甲亢性心脏病和评价缬沙坦治疗效果的指标之一。
Objective To investigate the changes of left ventricular remodeling and plasma brain natriuretic peptide in rats with thyroid hormone-induced cardiac disease and valsartan intervention to observe the cardioprotective effect of valsartan on hyperthyroid heart failure rats. Methods Forty Sprague-Dawley (SD) rats were randomly divided into control group, L-thyroxine group, valsartan low dose group (L-thyroxine +10 mg / kg valsartan) Large dose group (L-thyroxine +30 mg / kg valsartan). The hyperthyroidism model was established by intraperitoneal injection of L-thyroxine 0.5 mg / (kg · d) for 28 days in the thyroxine group and the valsartan intervention group, while the low dose valsartan group was given valsartan 10 mg / (kg. d) Gavage treatment, valsartan high-dose group valsartan 30 mg / (kg.d). Venous blood samples were taken before and after modeling. Serum T3 and T4 levels were determined by chemiluminescence assay. Brain natriuretic peptide (BNP) levels were measured by enzyme-linked immunosorbent assay. Left ventricular end-diastolic diameter (LVDD), left ventricular posterior wall (LVPW), and interventricular septum (IVS) thickness. Cardiac hypertrophy index was measured in the anatomical animals after cardiac echocardiography was performed. Left ventricular myocardium was collected and the morphology of left ventricular myocardium was observed by HE staining and Masson staining respectively. The left ventricular cell diameter and collagen volume fraction (collagen volume fraction, CVF). Results L-thyroxine 4 weeks after intraperitoneal injection can be successfully prepared hyperthyroid heart disease model, compared with the control group, L-thyroxine group left ventricular cavity expansion, wall thickening, cardiac index, myocardial cell diameter, collagen volume (P <0.01). The BNP level in the plasma of L-thyroxine group (776.61 ± 193.99) pg / mL was significantly higher than that of the control group (47.11 ± 23.19) pg / mL ) pg / mL and low dose group (371.64 ± 164.49) pg / mL were significantly lower than those in the untreated group (P <0.01). There was no significant difference in the above indexes between the valsartan large and small dose intervention groups . CONCLUSION Thyroxine can induce left ventricular myocyte hypertrophy, hyperplasia of matrix fibrosis, enlargement of ventricular cavity and increase of plasma BNP level. Valsartan can inhibit myocardial remodeling and decrease plasma BNP level. Plasma BNP level may be one of the indicators of early diagnosis of hyperthyroid heart disease and valsartan treatment.