ABC | Volume 110, Nº6, June 2018

Original Article Zhen et al AAC leads to obvious CH using 0.45 mm needle Arq Bras Cardiol. 2018; 110(6):568-576 Table 4 – Thickness of the left ventricle (mm) based on weight and needle size Weight 0.40 mm 0.45 mm 0.50 mm Sham 18 g 1.81 ± 0.30* 1.86 ± 0.17* 1.59 ± 0.09* 1.27 ± 0.07 22 g 1.69 ± 0.24* 1.55 ± 0.19* 1.22 ± 0.14 26 g 1.82 ± 0.30* 1.59 ± 0.22* 1.34 ± 0.07 Data are presented as the mean ± SD (n = 5). *p < 0.05 represents a significant difference between the abdominal aortic constriction (AAC) and sham groups. Death can occur after AAC. Undoubtedly, AAC increases cardiac afterloading. To cope with the additional biodynamics, the heart exerts a series of adaptive changes, including activation and hypertrophy of cardiomyocytes and hyperplasia of the extracellular matrix. 2 This compensational mechanism maintains cardiac output (CO) effectively for a period of time while maintaining the survival of the organism; it is also the basis for the establishment of the CH model. However, when the sudden afterloading is out of the range of cardiomyocyte adjustment, the bloodstream will be limited and cause constriction, resulting in AHF. AHF is typically characterized by rapid changes in heart failure (HF) symptoms. 3 Sato et al. 4 considered the incidence of death within 5 days as an assessment criterion of AHF. AHF could moderately or markedly improve by the second day if effectively controlled. AHF leads to high ventricular pressure, and high ventricular pressure leads to high pulmonary blood pressure, thus leading to pulmonary congestion, which is one of the causes of death after AAC. 5 Liao et al. 6 suggested that cardiogenic pneumo-edema is the main cause of postoperative death for PO mice. Additionally, arrhythmia may occur as part of the electrophysiological changes, 7 and cardiomyocyte sarcomeres may be disordered during the pathological changes. 8 These are all severe threats to the survival rate after AAC. Our record of mice death times (Table 1) showed the phenomenon of all deaths occurring within 5 days. A high incidence of death occurred during the initial 24h, which is in accordance with the aforementioned AHF criteria. In addition, there is a positive correlation between CO and BW; 9,10 therefore, compared with the low‑weight mice, high-weight mice require more CO and will have cardiac afterloading that is more increased than that of low-weight mice with the same aortic constriction. Results of the current study (Table 1) indicate that higher-weight mice had poorer tolerance for AAC, which is reflected in their mortality rates. Regarding mice with AAC that underwent ligation with a 0.40-mm needle, all mice in the 22-g and 26-g groups died. However, 6 out of 10 mice survived in the 18-g group. Figure 1 – Cardiomyocyte hypertrophy and collagen deposition histological examination. (A) Gross hearts under natural light. (B) The 20 × microscopic views of HE sections. (C) The 400 × microscopic views of HE sections. (D) Representative 200×microscopic views under standard lights of PSR sections in the interstitial space. (E) Representative 200 × microscopic views under standard lights of PSR sections in the perivascular space. Fibrosis is presented as red in the PSR sections. 572