Pressure Overload-induced Cardiac Hypertrophy Varies According to Different Ligation Needle Sizes and Body Weights in Mice

Abstract

BackgroundThe cardiac hypertrophy (CH) model for mice has been widely used, thereby providing an effective research foundation for CH exploration.ObjectiveTo research the effects of CH modeling under abdominal aortic constriction (AAC) using different needles and weights in mice.MethodsFour needles with different external diameters (0.35, 0.40, 0.45, and 0.50 mm) were used for AAC. 150 male C57BL/6 mice were selected according to body weight (BW) and divided into 3 weight levels: 18 g, 22 g, and 26 g (n = 50 in each group). All weight levels were divided into 5 groups: a sham group (n = 10) and 4 AAC groups using 4 ligation intensities (n = 10 per group). After surgery, survival rates were recorded, echocardiography was performed, hearts were dissected and used for histological detection, and data were statistically analyzed, P < 0.05 was considered statistically significant.ResultsAll mice died in the following AAC groups: 18g/0.35 mm, 22 g/0.35 mm, 26 g/0.35 mm, 22 g/0.40 mm, and 26 g/0.40 mm. All mice with AAC, those ligated with a 0.50-mm needle, and those that underwent sham operation survived. Different death rates occurred in the following AAC groups: 18 g/0.40 mm, 18 g/0.45 mm, 18 g/0.50 mm, 22 g/45 mm, 22 g/0.50 mm, 26 g/0.45 mm, and 26 g/0.50 mm. The heart weight/body weight ratios (5.39 ± 0.85, 6.41 ± 0.68, 4.67 ± 0.37, 5.22 ± 0.42, 4.23 ± 0.28, 5.41 ± 0.14, and 4.02 ± 0.13) were significantly increased compared with those of the sham groups for mice with the same weight levels.ConclusionA 0.45-mm needle led to more obvious CH than did 0.40-mm and 0.50-mm needles and caused extraordinary CH in 18-g mice.

Treg/Th17 Ratio Regulation May Play an Important Role in Epigallocatechin-3-Gallate–Mediated Attenuation of Increased Afterload-Induced Cardiac Hypertrophy

“…Cardiac hypertrophy begins 4 weeks after AAC, and heart failure is more severe at 8 weeks. 13 In this study, 6 weeks after the administration of EGCG was also 6-7 weeks after the AAC; it was found that the ventricular wall thickened and the ventricular cavity shrank during systole, and ejection fraction and fractional shortening increased, indicating that the heart was in the compensatory period of hypertrophy at this time.…”

“…In general, increased HW and HW/BW ratio are the main indicators of cardiac hypertrophy. 13 There was no significant difference in BW among the 3 groups (Table 1 ). The HW in the sham + vehicle group was lower than that in the AAC + vehicle and AAC + EGCG groups, whereas the HW in the AAC + EGCG group was lower than that in the AAC + vehicle group.…”

“…The model of increased afterload was constructed in C57BL/6 mice by abdominal aortic constriction (AAC) according to a previous study. 13 The mice fasted without food and water for 8 hours and 4 hours, respectively. Then, they were anesthetized with 10% of chloral hydrate (3 mL/kg, intraperitoneal injection) and fixed in the supine position.…”

Non-Coding RNAs in the Therapeutic Landscape of Pathological Cardiac Hypertrophy

“…A prolonged or persistent increase in hemodynamic demand, often, causes decompensated or pathological hypertrophy. Such chronic structural remodeling of the left ventricle (LV)—left ventricular hypertrophy (LVH)—is among the most robust driving forces for cardiovascular morbidity and mortality, being strongly associated with the development of chronic heart failure [ 8 , 9 , 10 ].…”