Table 3. Models of combined volume and pressure overload.
Method | Strengths | Limitations | Mouse | Rat | Rabbit | Dog | Sheep | Pig |
---|---|---|---|---|---|---|---|---|
Volume load + pulmonary hypertension | ||||||||
MCT + shunt | Vascular remodeling comparable to human PAH | Rapid RV decompensation | (137-143) | |||||
Time dependent progression of severe RV failure | Possible direct effects of MCT on the RV | |||||||
Chronic arterial-venous shunting | Physiology highly similar to PAH in adult ASD patients | Mild pulmonary hypertension | (144) | (145) | ||||
>6 months to develop pressure load | ||||||||
Shunt induced after birth | ||||||||
Fetal aorto-pulmonal shunt | Mimics pathophysiology of congenital shunts | Technically challenging surgical model | (146-151) | |||||
Only mild PAH and RV dysfunction | ||||||||
Volume load + pulmonary artery banding | ||||||||
Shunt + pulmonary artery banding | Precise volume and afterload increase | Need for open chest | (152) | |||||
Stable afterload, Adjustable | Only one study (in dogs) | |||||||
Wide range of RV strain | ||||||||
Pulmonary regurgitation + pulmonary artery banding | Physiology similar to patients with tetralogy of Fallot | Difficult | (74) | |||||
Need for open chest | ||||||||
Only one study (in pigs) |
An overview of models of Models of combined volume and pressure overload stratified to method of combined load increase and animal species. PAH, pulmonary arterial hypertension; MCT, monocrotaline.