Changes in cardiac structure and function in a modified rat model of myocardial hypertrophy

Abstract

SummaryAimIn this study we designed a modified method of abdominal aortic constriction (AAC) in order to establish a stable animal model of left ventricular hypertrophy (LVH). We also evaluated cardiac structure and function in rats with myocardial hypertrophy using echocardiography, and provide a theory and experimental basis for the application of drug interventions using the LVH animal model. We hope this model will provide insight into novel clinical therapies for LVH.MethodsThe abdominal aorta of male Wistar rats (80–100 g) was constricted between the branches of the coeliac and anterior mesenteric arteries, to a diameter of 0.55 mm. Echocardiography, using a linear phase array probe, combined with histology and plasma BNP concentration, was performed at three, four and six weeks post AAC.Results:The acute (24-hour) mortality rate was lower (8%) than in previous reports (15%) using this modified rat model. Compared with shams, animals who underwent AAC demonstrated significantly increased interventricular septal (IVS), LV posterior wall (LVPWd), LV mass index (LVMI), crosssectional area (CSA) of myocytes, and perivascular fibrosis; while the ejection fraction (EF), fractional shortening (FS) and cardiac output (CO) were consistently lower at each time interval. Notably, differences in these parameters between the AAC and sham groups were significant by three weeks and reached a peak at four weeks. Following AAC, plasma B-type natriuretic peptide (BNP) level was gradually elevated, compared with the sham group, between three and six weeks.ConclusionThis modified AAC model induced LVH both stably and safely by week four post surgery. Echocardiography was accurately able to assess changes in chamber dimensions and systolic properties in the rats with LVH.

Sprague-Dawley Rats Induced by Uninephrectomy, DOCA Injection, and Sodium Chloride: A Suitable Model for Chronic Hypertension with Cardiac Hypertrophy

“…Brain natriuretic peptide is a particular cardiac neurohormone that rises in response to myocardial hypertrophy and dilatation (Dai et al 2016). BNP, sometimes referred to as B-type NPs and a part of the natriuretic peptide (NP) system, is primarily released by cardiomyocytes in response to cardiac stretch and ischemia and is crucial for the function of the cardiorenal system (Okamoto et al 2019).…”

miR‐31‐5p suppresses myocardial hypertrophy by targeting Nfatc2ip

“…Most of them used an induction duration of more than 6 weeks, while a few focused on the early stage of cardiac hypertrophy. According to Wenjun Dai's work, 20 we used rats weighing 80–120 g to make up a 4‐week AAC‐induced cardiac hypertrophic model, which are younger rats rather than adults. Our data also showed that 4‐week induction by AAC showed significantly impaired cardiac function, increased heart size and cardiomyocyte size, and increased cardiac hypertrophic biomarkers Anp and b‐Mhc.…”

“…The abdominal aorta was occluded at the suprarenal level using a 2‐0 silk suture over a blunt 24‐G needle (the external diameter was 0.55 mm). 20 Rats were anaesthetised using 2% isoflurane (R510‐22‐16, RWD Life Science) and oxygen with a flow rate of 0.5 L/min and maintained with 1.5% isoflurane with an airflow of 0.3 L/min in an induction chamber connected with an animal anaesthesia machine. The sham groups ( n = 8) underwent similar surgery without placement of the aortic band.…”

Effect of Zoapatle (Montanoa tomentosa) on Inflammatory Markers in a Murine Model of Ventricular Hypertrophy

“…The heart was removed, weighed, and then cardiac dimensions were measured. For each animal, the cardiac index was calculated by dividing the weight of the heart by the body weight [43]. Also, samples of brain tissue, the left ventricle, and the renal cortex were collected.…”