Nayler W G, Panagiotopoulos S
Department of Medicine, University of Melbourne, Vic., Australia.
Am Heart J. 1993 Feb;125(2 Pt 2):626-9. doi: 10.1016/0002-8703(93)90213-s.
Calcium-dependent processes involved in atherosclerotic lesion formation include platelet aggregation, monocyte adhesion, release of growth factors, cell proliferation and migration, protein and collagen secretion and synthesis, and endothelial necrosis. In addition, the calcium (Ca2+) component of smooth muscle cell contraction contributes to one of the main risk factors, hypertension. The ability of the calcium channel blockers (CCBs) to interrupt the sequence of events that culminates in the formation of atherosclerotic lesions has been demonstrated in animal models and clinical trials. These studies have involved the short-acting CCBs. The results of this animal study show that manidipine, a new long-acting CCB, produces a dose-dependent reduction in atherosclerotic lesion formation without reducing plasma cholesterol.
参与动脉粥样硬化病变形成的钙依赖过程包括血小板聚集、单核细胞黏附、生长因子释放、细胞增殖与迁移、蛋白质和胶原蛋白的分泌与合成,以及内皮细胞坏死。此外,平滑肌细胞收缩的钙(Ca2+)成分是主要危险因素之一——高血压的成因。在动物模型和临床试验中已证实,钙通道阻滞剂(CCB)能够阻断最终导致动脉粥样硬化病变形成的一系列事件。这些研究涉及短效CCB。本动物研究结果表明,新型长效CCB马尼地平可使动脉粥样硬化病变形成呈剂量依赖性减少,且不降低血浆胆固醇水平。