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背景介绍病理性心肌肥厚是慢性心衰核心前驱病理改变持续交感神经过度激活是临床心衰典型特征。异丙肾上腺素(Isoproterenol,ISO)为非选择性β受体激动剂可模拟人体慢性交感亢进状态是常用造模工具。采用渗透泵缓释或低剂量连续皮下给药长期刺激心肌细胞、成纤维细胞与炎症细胞活化诱发心肌肥大、间质胶原沉积伴随ANP、BNP肥厚纤维化标志物升高。短期干预多形成代偿性肥厚延长刺激或提高剂量可进展为心室扩张、心功能下降的失代偿心衰模型。该模型无需复杂外科操作造模稳定、重复性佳广泛用于心肌重构、纤维化及药物干预机制研究。[1-2]图1.ISO对心肌细胞、成纤维细胞、炎症细胞的激活作用及促心肌纤维化效应 [1]ISO诱导动物心衰模型参考[2-5]案例1:小鼠心肌肥大选择8周龄的ICR远交系小鼠连续14天每天渗透泵皮下输注25mg/kg的ISO。案例2:大鼠心肌肥大选择6周龄的Wistar大鼠连续7天腹腔注射2 mg/kg的ISO。心肌肥大关键指标心脏重量指数升高、心肌细胞横截面积增大。案例3:小鼠慢性心衰选择6-8周龄的C57BL/6J小鼠连续14天皮下注射5 mg/kg的ISO。案例4:大鼠慢性心衰选择250-270g的SD大鼠连续7天皮下注射5 mg/kg的ISO。心衰关键指标左室射血分数、短轴缩短率显著降低。心衰诱导与治疗小分子推荐类型英文名称中文名称功能诱导心衰Isoprenaline hydrochloride盐酸异丙肾上腺素非选择性β受体激动剂Isoprenaline hemisulfate异丙肾上腺素半硫酸盐治疗药Propranolol普萘洛尔非选择性β受体拮抗剂Metoprolol美托洛尔选择性β₁受体拮抗剂Nebivolol hydrochloride盐酸奈必洛尔选择性β₁受体拮抗剂Pirfenidone吡非尼酮多通路广谱抗纤维化参考文献[1] Zhang Kehui, et al. A Novel Orally Bioavailable PI3K/HDAC Dual Inhibitor Induces Programmed Cell Death Through Synergistic c-MYC Downregulation. Chinese Chemical Letters, 2026, Journal pre-proof.[2] Kim Seong Hoon, et al. Chlorogenic Acid Attenuates Cardiac Hypertrophy and Fibrosis by Downregulating Galectin 3. Scientific Reports, vol. 15, 2025, p. 26925.[3] Teixeira Larissa B., et al. Ang-(1-7) Is an Endogenous β-Arrestin-Biased Agonist of the AT₁ Receptor with Protective Action in Cardiac Hypertrophy. Scientific Reports, vol. 7, 2017, p. 11903.[4] Wang Yaojiang, et al. Heart Failure Induced by Isoproterenol: A Comparison of Two Doses and Two Delivery Methods in C57BL/6J Mice. PLOS ONE, vol. 20, no. 11, 2025, e0334880.[5] Huang Yujing, et al. MiR-21-3p Inhibitor Exerts Myocardial Protective Effects by Altering Macrophage Polarization State and Reducing Excessive Mitophagy. Communications Biology, vol. 7, 2024, p. 1371.来自于公开发表的文献仅供参考所有产品仅用于工业应用或者科学研究等非医疗目的不可用于人类或动物的临床诊断或治疗非药用非食用 让小鼠“心碎”，科学家是怎么做到的？
背景介绍病理性心肌肥厚是慢性心衰核心前驱病理改变持续交感神经过度激活是临床心衰典型特征。异丙肾上腺素(Isoproterenol,ISO)为非选择性β受体激动剂可模拟人体慢性交感亢进状态是常用造模工具。采用渗透泵缓释或低剂量连续皮下给药长期刺激心肌细胞、成纤维细胞与炎症细胞活化诱发心肌肥大、间质胶原沉积伴随ANP、BNP肥厚纤维化标志物升高。短期干预多形成代偿性肥厚延长刺激或提高剂量可进展为心室扩张、心功能下降的失代偿心衰模型。该模型无需复杂外科操作造模稳定、重复性佳广泛用于心肌重构、纤维化及药物干预机制研究。[1-2]图1.ISO对心肌细胞、成纤维细胞、炎症细胞的激活作用及促心肌纤维化效应 [1]ISO诱导动物心衰模型参考[2-5]案例1:小鼠心肌肥大选择8周龄的ICR远交系小鼠连续14天每天渗透泵皮下输注25mg/kg的ISO。案例2:大鼠心肌肥大选择6周龄的Wistar大鼠连续7天腹腔注射2 mg/kg的ISO。心肌肥大关键指标心脏重量指数升高、心肌细胞横截面积增大。案例3:小鼠慢性心衰选择6-8周龄的C57BL/6J小鼠连续14天皮下注射5 mg/kg的ISO。案例4:大鼠慢性心衰选择250-270g的SD大鼠连续7天皮下注射5 mg/kg的ISO。心衰关键指标左室射血分数、短轴缩短率显著降低。心衰诱导与治疗小分子推荐类型英文名称中文名称功能诱导心衰Isoprenaline hydrochloride盐酸异丙肾上腺素非选择性β受体激动剂Isoprenaline hemisulfate异丙肾上腺素半硫酸盐治疗药Propranolol普萘洛尔非选择性β受体拮抗剂Metoprolol美托洛尔选择性β₁受体拮抗剂Nebivolol hydrochloride盐酸奈必洛尔选择性β₁受体拮抗剂Pirfenidone吡非尼酮多通路广谱抗纤维化参考文献[1] Zhang Kehui, et al. A Novel Orally Bioavailable PI3K/HDAC Dual Inhibitor Induces Programmed Cell Death Through Synergistic c-MYC Downregulation. Chinese Chemical Letters, 2026, Journal pre-proof.[2] Kim Seong Hoon, et al. Chlorogenic Acid Attenuates Cardiac Hypertrophy and Fibrosis by Downregulating Galectin 3. Scientific Reports, vol. 15, 2025, p. 26925.[3] Teixeira Larissa B., et al. Ang-(1-7) Is an Endogenous β-Arrestin-Biased Agonist of the AT₁ Receptor with Protective Action in Cardiac Hypertrophy. Scientific Reports, vol. 7, 2017, p. 11903.[4] Wang Yaojiang, et al. Heart Failure Induced by Isoproterenol: A Comparison of Two Doses and Two Delivery Methods in C57BL/6J Mice. PLOS ONE, vol. 20, no. 11, 2025, e0334880.[5] Huang Yujing, et al. MiR-21-3p Inhibitor Exerts Myocardial Protective Effects by Altering Macrophage Polarization State and Reducing Excessive Mitophagy. Communications Biology, vol. 7, 2024, p. 1371.来自于公开发表的文献仅供参考所有产品仅用于工业应用或者科学研究等非医疗目的不可用于人类或动物的临床诊断或治疗非药用非食用