Abdominal Aortic Constriction (AAC) Model

Model Description

The AAC model induces pressure-overload heart failure by increasing systemic vascular resistance, replicating key stages of human cardiac remodeling from compensated hypertrophy to decompensated failure. Recognized for its high clinical relevance, this model is ideal for:

• Pathophysiological studies: Neurohormonal activation (RAAS, ANP/BNP)
• Molecular mechanism exploration: Myocardial fibrosis, apoptosis pathways
• Drug development: Cardioprotective agents, antihypertensives

 Model Flexibility:
✓ Hypertrophy phase: 4-6 weeks post-AAC
✓ Failure phase: 8-12 weeks post-AAC

Applications

• Cardiac hypertrophy-to-failure transition studies
• Anti-fibrotic drug efficacy evaluation
• Biomarker discovery (NT-proBNP, troponin I)
• Gene therapy validation (CRISPR-based interventions)

Modeling Protocol —— Microsurgical AAC Induction

1. Surgical Steps:

• Midline laparotomy under isoflurane anesthesia
• Aortic exposure: Isolate suprarenal abdominal aorta
• Constriction: Ligate aorta over a 21G needle (0.8mm outer diameter) → Remove needle → 60-70% lumen reduction
• Close abdomen with 4-0 sutures

2. Post-op Monitoring:

Weekly echocardiography ∙ Terminal hemodynamic assessment

Validation & Testing

Technical Advantages