Ferdinal Frans, Suyatna Franciscus D, Wanandi Septelia I, Sadikin Mohammad
Department of Biochemistry and Molecular Biology, Faculty of Medicine, Tarumanagara University, Jl.Letjen S. Parman no.1, Jakarta 11440, Indonesia.
Acta Med Indones. 2010 Jul;42(3):135-41.
to explore the effects of chronic systemic hypoxia on myocardial structure and morphology. In addition, the goal of present study is to develop a hypoxia-induced heart failure model in rats.
Sprague-Dawley male rats, weighing 220-250 g at the time of recruitment were randomly allocated into 7 groups (n = 4 per group), the control normoxia group was exposed to room air, while the hypoxia groups were caged in a plexiglas hypoxic chamber (8% O2 and 92% N2) for 28 days. Structural and morphological changes of ventricular myocardium were determined at day 28, while blood gas parameters were measured at day 1, 3, 7, 14, 21, and 28.
histopathologic and morphologic evaluation showed massive hypertrophy accompanied by damage of the intercalated disk (ID) structure, angiogenesis, necrosis, fibrosis, and apoptosis as a hallmark of ventricular remodeling. At the end of treatment, there were increases of LV (2.79 vs 3.71) and RV (1.72 vs 2.54) wall thicknesses, and also in hypertrophy index (from 3.19 to 5.74). Blood gas analysis revealed metabolic acidosis compensated by respiratory alkalosis. There was an observed decrease of blood gas parameters in hypoxia group compared to control group: PO2 (24.7 vs 96.4 mm Hg), PCO2 (18.2 vs 40.4 mm Hg), O2 saturation (25.5 vs 94.1 %), and HCO3 (10.1 vs 23.4 mmol/L). On the other hand an increase in hemoglobin level (221.5 vs 120.3 g/L), haematocrit level (68.6 vs 45.2 %), and red blood cell count (10.4 vs 6.9 μL/1000) could be observed.
our data clearly show that chronic systemic hypoxia causes massive ventricular hypertrophy accompanied by severe structural and morphological impairment of ventricular myocardium, which eventually results in cardiac failure.
探讨慢性全身性缺氧对心肌结构和形态的影响。此外，本研究的目的是建立大鼠缺氧诱导的心力衰竭模型。
招募体重220 - 250 g的雄性Sprague-Dawley大鼠，随机分为7组（每组n = 4），对照常氧组暴露于室内空气，而缺氧组置于有机玻璃缺氧箱（8%氧气和92%氮气）中28天。在第28天测定心室心肌的结构和形态变化，在第1、3、7、14、21和28天测量血气参数。
组织病理学和形态学评估显示大量心肌肥大，伴有闰盘（ID）结构损伤、血管生成、坏死、纤维化和凋亡，这些是心室重构的标志。治疗结束时，左心室（2.79 vs 3.71）和右心室（1.72 vs 2.54）壁厚度增加，肥大指数也增加（从3.19增至5.74）。血气分析显示代谢性酸中毒由呼吸性碱中毒代偿。与对照组相比，缺氧组的血气参数下降：氧分压（24.7 vs 96.4 mmHg）、二氧化碳分压（18.2 vs 40.4 mmHg）、氧饱和度（25.5 vs 94.1%）和碳酸氢根（10.1 vs 23.4 mmol/L）。另一方面，可观察到血红蛋白水平（221.5 vs 120.3 g/L）、血细胞比容水平（68.6 vs 45.2%）和红细胞计数（10.4 vs 6.9 μL/1000）升高。
我们的数据清楚地表明，慢性全身性缺氧导致大量心室肥大，伴有心室心肌严重的结构和形态损害，最终导致心力衰竭。
