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采用免疫组化,图像分析,细胞培养和细胞内游离钙离子浓度([Ca2+]i)测定等方法研究2,6-二甲基-4-(2-氯苯基)-1,4-二氢-3,5-吡啶二羧酸二甲酯(DCDDP)防治野百合碱(MCT)所致肺动脉高压的作用机理.结果发现每天ipDCDDP5-500μg·kg-11次,连续28d,能够明显地减少MCT(60mg·kg-1sc)引起的大鼠肺组织中5-HT相对含量及其受体阳性细胞数目增多,对5-HT引起的肺动脉平滑肌细胞增生,收缩及其[Ca2+]i增高都有显著的抑制作用.结果提示,抑制肺组织中5-HT含量及其受体数目的增加,对抗5-HT引起的血管平滑肌细胞增生及收缩,可能是DCDDP防治MCT性肺动脉高压的重要机理之一.
Immunohistochemistry, image analysis, cell culture and intracellular free calcium concentration ([Ca2 +] i) determination of 2,6-dimethyl-4- (2-chlorophenyl) -1,4-bis Hydrogen-3,5-pyridinedicarboxylate (DCDDP) prevents and controls the mechanism of action of monocrotaline (MCT) -induced pulmonary hypertension. The results showed that ipDCDDP5-500μg · kg-11 times a day for 28 consecutive days, can significantly reduce the MCT (60mg · kg-1sc) -induced rat lung tissue relative content of 5-HT and its receptor positive cells increased, 5 -HT induced pulmonary artery smooth muscle cell proliferation, contraction and its [Ca2] i increased significantly inhibited. The results suggest that inhibition of 5-HT content and its receptor number in lung tissue may be one of the important mechanisms of DCDDP in preventing and treating MCT pulmonary hypertension by inhibiting 5-HT-induced proliferation and contraction of vascular smooth muscle cells.