Nogueira Breno V, Peotta Veronica A, Meyrelles Silvana S, Vasquez Elisardo C
Laboratory of Transgenes and Cardiovascular Control, Physiological Sciences Graduate Program, Health Sciences Center, Federal University of Espirito Santo, Vitoria, ES, Brazil.
Arch Med Res. 2007 Nov;38(8):816-21. doi: 10.1016/j.arcmed.2007.06.005. Epub 2007 Aug 2.
The apolipoprotein E-deficient mouse (ApoE) spontaneously develops hypercholesterolemia and atherosclerotic lesions in large arteries. It is also known that angiotensin II-induced hypertension accelerates the development of atherosclerosis in ApoE mice. The objective of this study was to evaluate the aortic remodeling process in ApoE mice during the early phase of atherosclerosis in two-kidney one-clip hypertensive (2K1C) mice and in mice with the coexistence of atherosclerosis and arterial hypertension.
Renovascular hypertension was induced in 8- to 9-week-old C57BL/6 (C57) and ApoE and compared to sham animals 28 days later. C57-2K1C and ApoE-2K1C mice showed hypertension, tachycardia, and cardiac hypertrophy of similar magnitude.
ApoE and ApoE-2K1C mice showed high levels of plasma cholesterol (4.8- and 3.6-fold) and aorta lipid deposition (85- and 101-fold) compared to C57 mice. The aorta lumen area was increased in C57-2K1C and ApoE-2K1C mice (0.57 +/- 0.04 and 0.55 +/- 0.02 mm(2)) compared to C57 mice (0.50 +/- 0.02 mm(2), p <0.05). The aorta wall area was increased by 20% in C57-2K1C and by 12% in ApoE-2K1C mice compared to C57 and ApoE.
The main finding of this study was the absence of aorta remodeling in ApoE mice at the early stage of atherosclerosis and an outward remodeling of similar magnitude in C57-2K1C and ApoE-2K1C mice.
载脂蛋白E缺陷小鼠(ApoE)会自发出现高胆固醇血症,并在大动脉中形成动脉粥样硬化病变。此外,已知血管紧张素II诱导的高血压会加速ApoE小鼠动脉粥样硬化的发展。本研究的目的是评估两肾一夹高血压(2K1C)小鼠以及动脉粥样硬化与动脉高血压并存的小鼠在动脉粥样硬化早期阶段ApoE小鼠的主动脉重塑过程。
在8至9周龄的C57BL/6(C57)小鼠和ApoE小鼠中诱导肾血管性高血压,并在28天后与假手术动物进行比较。C57-2K1C和ApoE-2K1C小鼠表现出相似程度的高血压、心动过速和心脏肥大。
与C57小鼠相比,ApoE和ApoE-2K1C小鼠的血浆胆固醇水平(分别为4.8倍和3.6倍)和主动脉脂质沉积(分别为85倍和101倍)较高。与C57小鼠(0.50±0.02平方毫米)相比,C57-2K1C和ApoE-2K1C小鼠的主动脉管腔面积增加(分别为0.57±0.04和0.55±0.02平方毫米,p<0.05)。与C57和ApoE小鼠相比,C57-2K1C小鼠的主动脉壁面积增加了20%,ApoE-2K1C小鼠增加了12%。
本研究的主要发现是,在动脉粥样硬化早期阶段,ApoE小鼠不存在主动脉重塑,而C57-2K1C和ApoE-2K1C小鼠存在相似程度的向外重塑。