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. 2020 Feb 10;10(1):2045894019897513. doi: 10.1177/2045894019897513

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© The Author(s) 2020

Creative Commons CC-BY: This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Fig. 4. — RV end-systolic volume index (RVESVI) (a), RV end-diastolic volume index (RVEDVI) (b), RV mass index (c), RV ejection fraction (RVEF) (d), ventricular mass index (VMI) (e), and Stroke volume index (SVI) (f) in normoxia (n = 8), five week Sugen–hypoxia (n = 4) and eight week Sugen–hypoxia (n = 4). RV end-diastolic and end-systolic volumes and RV mass were determined by manual planimetry and indexed to body surface area. RVEF was determined by ((RVEDV – RVESV)/RVEDV) × 100%. A demonstrates progressive increase in RV end-systolic volume index during the course of Sugen–hypoxia, while B demonstrates RV dilatation at eight weeks. RV mass index (c) was significantly increased in five week and eight week Sugen–hypoxia compared to normoxic rats. RVEF (d) was preserved, however, trending toward deterioration at eight weeks. Ventricular mass index (VMI) was calculated as the ratio between RV mass to LV mass. Interventricular septum was considered as part of the LV. VMI maybe an alternative to RV/(LV + septum) measured at autopsy as discussed. Results demonstrated increased VMI at five weeks and eight weeks of Sugen–hypoxia compared to normoxic rats (e). There were no significant differences in stroke volume index (SVI) between normoxia, five week Sugen–hypoxia and eight week Sugen–hypoxia (f). Results are shown as mean ± SEM. The groups were compared by ANOVA and if there was statistical significance, a Tukey HSD test was used for post hoc.

LV: left ventricle; RV: right ventricle; SuHx: Sugen–hypoxia.