异搏定对缺氧和缩血管物质促肺动脉平滑肌细胞增生的影响

The Effect of Verapamil on the Proliferation of Smooth Muscle Cells of Porcine Pulmonary Artery Induced by Hypoxia and Vasoconstructors

采用~３Ｈ－ＴｄＲ掺入、结晶紫染色以及ＰＣＮＡ免疫细胞化学方法观察异搏定对缺氧和４种缩血管物质促肺动脉平滑肌细胞增生的影响。结果发现：①４种缩血管物质（ＥＴ－１、ＡＴⅡ、Ａ_（２３１７８）、ＫＣｌ）均有不同程度的促肺动脉平滑肌细胞（ＰＡＳＭＣ）ＤＮＡ合成的作用，其作用可被Ｃａ^（２＋）通道阻滞剂异搏定阻断；②缺氧所致ＰＡＳＭＣ增殖的３项指标变化同样可被异搏定阻断。表明［Ｃａ^（２＋）］ｉ升高可能为缺氧和缩血管物质引起肺血管ＳＭＣ收缩和增生的信息传递的共同途径。

The effects of verapamil on the proliferation of cultured pulmonary arterial smooth muscle cells (PASMC) induced by hypoxia and four vasoconstructors (ET-1, ATⅡ A_(23187), KCl) were studied by using crystal violet staining, ~3H-TdR incorporation and proliferating cell nuclear antigen (PCNA) immunocytochemical methods. The results showed: (1) The four vasoconstructors could induce the DNA systhesis of PASMC seperately, which could be inhibited by verapamil. (2) The proliferation of PASMC induced by hypoxia could also be inhibited by verapamil. These results suggested that the increase in [Ca^(2+)]i might be the common signal transduction pathway of the constriction and proliferation of PASMC induced by hypoxia and these vasoconstructors.