Fitscha P, Rauscha F, O'Grady J, Keiler A, Sinzinger H
2nd Department of Internal Medicine, Policlinic Vienna, Austria.
Exp Toxicol Pathol. 1994 Mar;46(1):75-80. doi: 10.1016/S0940-2993(11)80024-2.
The anti-mitotic (3H-thymidine uptake quantified using autoradiography) and anti-proliferative (counting of activated smooth muscle cells on semithin sections) effects of the dihydropyridine calcium channel blocker isradipine (0.3 mg/kg) have been assessed in a rabbit arterial stress model. Isradipine caused a significant drop in both mitotic and proliferative activity. These effects were more pronounced by pretreatment (6 hours before lesion induction with desoxycorticosterone) with isradipine as compared to posttreatment (6 hours after experimental lesioning). The benefit induced by isradipine was abolished by aspirin treatment. In-vitro vascular prostacyclin formation and cholesterol content were not affected. These findings suggest that the anti-atherosclerotic action of isradipine on mitotic activity and cellular proliferation is mediated by a cyclooxygenase product, most likely via enhanced local vascular PGI2-synthesis.
在兔动脉应激模型中，已评估了二氢吡啶类钙通道阻滞剂伊拉地平（0.3毫克/千克）的抗有丝分裂作用（使用放射自显影法定量3H-胸腺嘧啶核苷摄取）和抗增殖作用（在半薄切片上计数活化的平滑肌细胞）。伊拉地平导致有丝分裂和增殖活性显著下降。与治疗后（实验损伤后6小时）相比，预处理（用脱氧皮质酮诱导损伤前6小时）伊拉地平，这些作用更明显。阿司匹林治疗消除了伊拉地平诱导的益处。体外血管前列环素形成和胆固醇含量未受影响。这些发现表明，伊拉地平对有丝分裂活性和细胞增殖的抗动脉粥样硬化作用是由环氧化酶产物介导的，很可能是通过增强局部血管前列环素2的合成。
