血管再阻塞是氣球擴張手術成功後最主要的失敗原因，再阻塞是由於受傷血管平滑肌增生所造成的，因此調節血管平滑肌細胞的生長就具有治療的意義。Zanidip®是新1,4-dihydropyridine骨架的 L型鈣離子管道阻斷劑，在臨床被用於治療高血壓疾病。本篇論文的目的在評估Zanidip®在體外實驗是否能有效抑制大鼠血管平滑肌細胞增生，並同時進行體內實驗評估此藥是否能改善氣球擴張手術後所造成的血管再阻塞。
在體外實驗中，我們評估Zanidip®對於大鼠血管平滑肌的增生作用，由錐藍排除法（trypan blue exclusion assay）實驗證實，Zanidip®可抑制胎牛血清（FBS）誘導的血管平滑肌細胞增生，並且呈現劑量相關性。由流式細胞分析實驗顯示，Zanidip®顯著性地降低血管平滑肌細胞S期及提高G0 /G1期；除此之外，Zanidip®也會降低血小板衍生的生長因子（PDGF）誘導血管平滑肌細胞內的鈣離子濃度增加。在活體動物實驗，Zanidip®經由減低氣球擴張術誘發頸動脈血管新生內層的產生，而具有抑制血管內膜增厚作用。結論：由實驗結果顯示，將來Zanidip®可能用於治療氣球擴張術、支架置入及冠狀動脈繞道手術後的血管再阻塞的臨床病人。

Restenosis, or renarrowing of the artery shortly after percutaneous transluminal coronary angioplasty, is a major limitation to the success of the procedure and is due mainly to smooth muscle cell accumulation in the artery wall at the site of balloon injury. Therefore, modulation of vascular smooth muscle cells (VSMCs) growth has critical therapeutic implications. Zanidip®, a new 1,4-dihydropyridine L-type calcium channel antagonist, used for the treatment of hypertension in clinical. The purpose of this study is to estimate whether Zanidip® might be efficient for inhibiting the proliferation of rat VSMCs in vitro and restenosis after balloon angioplasty in vivo.
We evaluated the in vitro effect of Zanidip® on proliferation of cultured rat VSMCs. We showed that Zanidip® significantly inhibited 10% fetal bovine serum (FBS)-induced VSMCs proliferation in a concentration-dependent manner, as demonstrated by trypan blue exclusion. Flow cytometry studies revealed that Zanidip® significantly decreased S phase and elevated G0/G1 phase of VSMCs. In addition, Zanidip® also decreased the PDGF-induced calcium rise in VSMCs. In vivo, Zanidip® has an inhibitory effect on intimal thickening by attenuating intimal VSMCs proliferation. Our results suggest that Zanidip®  may in clinical patient who suffered from restenosis after PTCA, in-stent, coronary artery bypass in the future.