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Updated: Jul 17, 2026
Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
Published on: July 14, 2021
Histopathological study of time course changes in inter-renal aortic banding-induced left ventricular hypertrophy of
Hiroyuki Higashiyama1, Masaki Sugai, Hirotaka Inoue
1Pharmacology Department, Tsukuba Research Laboratories, GlaxoSmithKline KK, Ibaraki, Japan.
Insights
Pressure overload causes left ventricular hypertrophy (LVH) primarily through early coronary artery changes, not cardiomyocyte growth. This study details the timeline of these vascular alterations in a mouse model.
Area of Science:
- Cardiovascular pathology
- Animal models of cardiac disease
- Vascular biology
Background:
- Left ventricular hypertrophy (LVH) is a significant risk factor for cardiac morbidity and mortality.
- Understanding the temporal sequence of histopathological changes in pressure overload-induced LVH is crucial.
Purpose of the Study:
- To investigate the time course of histopathological alterations in the left ventricle during pressure overload-induced LVH.
- To characterize early vascular changes in the coronary arteries and arterioles.
Main Methods:
- Aortic banding was performed on mice to induce LVH.
- Histopathological and immunohistochemical analyses were conducted at multiple time points (3-42 days post-banding).
- Stains included H&E, Masson's trichrome, and immunohistochemistry for PCNA, aSMA, ICAM-1, type I collagen, and CD31.
Main Results:
- Early (3 days) acute inflammatory changes and ICAM-1 expression were observed in coronary arteries/arterioles.
- Vascular wall thickening and fibrosis in coronary arteries/arterioles were noted after day 10, with smooth muscle cell proliferation.
- Minimal cardiomyocyte hypertrophy was observed at the light microscope level after day 28.
Conclusions:
- Histopathological alterations in early pressure overload LVH are predominantly vascular, affecting coronary arteries and arterioles.
- These early vascular changes are likely hypertension-related.
- Cardiomyocyte hypertrophy is a later and minimal finding in this model at the light microscope level.
Abstract:
The left ventricular hypertrophy (LVH) in response to pressure overload is an important risk factor in cardiac morbidity and mortality. To investigate the time course of histopathological alterations in the LVH in response to pressure overload, histopathological and immunohistochemical examination was performed using the aortic banding-induced mouse LVH model. Five-week-old male CD-1 mice were subjected to the inter-renal aortic banding. Major organs were sampled on 3, 10, 14, 21, 28 or 42 days after banding. Haematoxylin and eosin (H&E) staining, Masson's trichrome staining and immunohistochemistry for proliferating cell nuclear antigen (PCNA), alpha-smooth muscle actin (aSMA), ICAM-1, type I collagen and CD31 was performed and microscopically examined. Three days after aortic banding, acute inflammatory changes, such as macrophages/neutrophil infiltration and vascular wall injury were observed on/around the coronary arteries/arterioles of both ventricles. Intense ICAM-1 immunostaining was observed on the endothelium of the coronary arteries/arterioles. After day 10, vascular wall thickening and perivascular fibrosis was induced on the coronary arteries/arterioles. Immunohistochemistry for aSMA and PCNA demonstrated the proliferation of vascular smooth muscle cells in the media. After day 28, minimal cardiomyocyte hypertrophy was observed at the light microscope level. In the inter-renal aortic banding LVH model, histopathological alterations in early phase were mainly observed on coronary arteries/arterioles. These early phase alterations were thought to be hypertension-related changes in the coronary vasculatures. The cardiomyocyte hypertrophy observed in later phase was minimal at the light microscope level. These evidences would facilitate the understanding of pathophysiology of pressure overload LVH.
