Galle J, Bassenge E
Lehrstuhl für Angewandte Physiologie, Universität Freiburg.
Z Kardiol. 1991;80 Suppl 9:15-20.
Investigations of circulation in humans and various animal models demonstrate changes in the reactivity of atherosclerotic arteries. Both attenuation of endothelium-dependent vasodilations and enhancement of contractile responses to different contractile agonists have been described. Recent in vitro studies provide evidence that low-density lipoproteins (LDL) accumulating in atherosclerotic arteries are involved in the mechanisms responsible for these changes. Perfusion of isolated arteries with native and oxidatively modified LDL results in attenuation of endothelium-dependent dilations. Furthermore, oxidized LDL impairs dilations to endothelium-independent agonists, and potentiates agonist-induced contractile responses. These in vitro observations are in accordance with alterations of the reactivity of arteries obtained from cholesterol fed rabbits. In these atherosclerotic arteries, contractile responses to the same agonists as used in the in vitro studies were enhanced, and endothelium-dependent dilations were attenuated. The extent of these changes was positively correlated with the degree of intimal atherosclerotic plaques, thus, with the regions containing oxidized LDL. Therefore, accumulation of oxidized LDL in atherosclerotic arteries may lead to an imbalance of vascular tonus regulation which favors inadequate vasoconstriction.
对人类和各种动物模型的循环系统研究表明，动脉粥样硬化动脉的反应性会发生变化。内皮依赖性血管舒张功能减弱以及对不同收缩性激动剂的收缩反应增强均有相关描述。最近的体外研究表明，在动脉粥样硬化动脉中积聚的低密度脂蛋白（LDL）参与了导致这些变化的机制。用天然和氧化修饰的LDL灌注离体动脉会导致内皮依赖性舒张功能减弱。此外，氧化型LDL会损害对非内皮依赖性激动剂的舒张反应，并增强激动剂诱导的收缩反应。这些体外观察结果与喂食胆固醇的兔子的动脉反应性变化一致。在这些动脉粥样硬化动脉中，对与体外研究中使用的相同激动剂的收缩反应增强，内皮依赖性舒张功能减弱。这些变化的程度与内膜动脉粥样硬化斑块的程度呈正相关，因此与含有氧化型LDL的区域呈正相关。因此，氧化型LDL在动脉粥样硬化动脉中的积聚可能导致血管张力调节失衡，从而有利于不适当的血管收缩。
