Saladino C F, Schneider M, Jonas E A, Grimes G
Department of Medicine, Nassau County Medical Center, East Meadow, NY 11554.
Artery. 1992;19(5):297-306.
We have shown previously that parenterally-administered lipid emulsions can be utilized to induce early atherosclerosis in the aortas of Sprague-Dawley rats. In order to evaluate the effect of obesity on lipid-induced atherogenesis, we have utilized this same approach in the present study to demonstrate that i.v. infusions of the parenteral lipid emulsion, Lipofundin-S, will induce in the genetically obese Zucker rat and its lean littermate aortic endothelial and myofibroelastic changes indicative of early atherogenesis. Four groups of rats were used: 1) obese controls, 2) obese lipid-infused, 3) lean littermate controls, and 4) lean littermate lipid-infused. Observations were made with light and transmission electron microscopy (TEM), using qualitative morphological criteria to evaluate the results. Based on the fact that both untreated control and Lipofundin-S-induced atherosclerosis was more frequent and generally more advanced in the obese animals than in their respective lean counterparts, it appears that the obese Zucker rat is more susceptible to both spontaneous and hyperlipidemia-induced atherosclerosis than its respective lean littermate. Thus, obesity in these animals, as might be the case in humans, could potentiate an atherogenic process already enhanced by hyperlipidemia.
我们之前已经表明，肠胃外给药的脂质乳剂可用于在斯普拉格-道利大鼠的主动脉中诱导早期动脉粥样硬化。为了评估肥胖对脂质诱导的动脉粥样硬化形成的影响，在本研究中我们采用了相同的方法来证明，静脉输注肠胃外脂质乳剂Lipofundin-S会在遗传性肥胖的 Zucker 大鼠及其瘦的同窝仔鼠中诱导出表明早期动脉粥样硬化形成的主动脉内皮和肌纤维弹性变化。使用了四组大鼠：1）肥胖对照组，2）肥胖脂质输注组，3）瘦的同窝仔鼠对照组，以及4）瘦的同窝仔鼠脂质输注组。使用光镜和透射电子显微镜（TEM）进行观察，采用定性形态学标准来评估结果。基于未治疗的对照组和Lipofundin-S诱导的动脉粥样硬化在肥胖动物中比在其各自的瘦的对应动物中更频繁且通常更严重这一事实，看来肥胖的 Zucker 大鼠比其各自瘦的同窝仔鼠更容易患自发性和高脂血症诱导的动脉粥样硬化。因此，这些动物中的肥胖，就像人类的情况一样，可能会增强已经由高脂血症加剧的动脉粥样硬化过程。
