Histopathological study of time course changes in inter‐renal aortic banding‐induced left ventricular hypertrophy of mice

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.

Partial nephrectomy as a model for uremic cardiomyopathy in the mouse

“…In general, the physiological, morphological, and biochemical alterations with PNx were similar to that which we have reported in the male SpragueDawley rat, where suprarenal aortic constriction was used as a control for hypertensive changes (5). Interestingly, the CD1 mouse also develops severe hypertension with suprarenal aortic constriction but very little cardiac hypertrophy or fibrosis over a similar time course to what we employed in our current study (4,17). Moreover, in the current study, "triple" antihypertensive therapy (15) substantially lowered blood pressure toward normal, but it did not attenuate the cardiac hypertrophy or fibrosis induced by PNx.…”

Modulation of actin isoform expression before the transition from experimental compensated pressure-overload cardiac hypertrophy to decompensation

“…In AC 2 animals, the expression of this protein was significantly higher than both C and AC 1 . In accordance with recent data obtained in mice with interrenal aortic banding (11,15), the marked increase in SMA expression in long-lasting pressure overload could be mainly attributed to the proliferation/hypertrophy of vascular smooth muscle cells in the media, typical hypertension-related change in resistant vessels including the coronary arteries. Alpha-SMApositive cells in the adventitia and perivascular regions, attributable to differentiation of fibroblasts into myofibroblasts (16), were negligible in both AC groups.…”

Bone Marrow Support of the Heart in Pressure Overload Is Lost with Aging

“…Several studies have characterized the inflammatory cell response in pressure overload in young animals [20], [23]. Xia et al demonstrated no significant neutrophil infiltration following TAC and a peak infiltration of macrophages within 2 weeks which subsided by 28 days.…”