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目的：探讨尼群地平（ Ｎ Ｉ Ｔ）对野百合碱（ Ｍ Ｃ Ｔ）性肺动脉高压的防治作用机理． 方法：用免疫组化方法和图像分析技术测定肺组织中五羟色胺（５ Ｈ Ｔ）及其受体的变化；采用 Ｍ Ｔ Ｔ 法和测微网及钙荧光指示剂 Ｆｕｒａ ２／ Ａｍ 测定培养的肺动脉平滑肌细胞（ Ｐ Ａ Ｓ Ｍ Ｃ）生长情况和收缩功能以及细胞内游离 Ｃａ２＋ 浓度． 结果：发现 Ｎ Ｉ Ｔ 能够显著地抑制 Ｍ Ｃ Ｔ 引起的５ Ｈ Ｔ 及其受体阳性细胞数目的增加和相对含量的增多．使５ Ｈ Ｔ及其受体阳性细胞数目从（１２７ ４９４±２０ ７３６）／ｍ ｍ ２和（１４ ６２４±３ ０１０）／ｍ ｍ ２ 分别减少到（２３ ８１４±１３ ２８４）／ｍ ｍ ２和（ ４ ８７５±９７２）／ｍ ｍ ２（ Ｐ＜ ０．０１）． 对５ Ｈ Ｔ引起培养的 Ｐ Ａ Ｓ Ｍ Ｃ增生和收缩都有显著的抑制作用． 这种抑制作用与其阻断５ Ｈ Ｔ 引起的 Ｃａ２＋ 内流有关． 结论： Ｎ Ｉ Ｔ不仅具有对抗５ Ｈ Ｔ的收缩血管作用和促 Ｐ Ａ Ｓ Ｍ Ｃ增殖作用， 而且还能抑制 Ｍ Ｃ Ｔ性肺动脉高压时肺组织中 ５ Ｈ Ｔ 阳性细胞的数量和 ５ Ｈ Ｔ 相对含量，这是 Ｎ Ｉ Ｔ 防治 Ｍ Ｃ Ｔ 性肺动脉高压的重要机制之一．
Objective: To investigate the preventive and therapeutic mechanism of nitrendipine (N I T) on monocrotaline-induced pulmonary hypertension. Methods: The changes of serotonin (5H T) and its receptors in lung tissue were determined by immunohistochemistry and image analysis techniques. The levels of 5H T and its receptors in lung tissue were determined by MTT method and Fura 2 / Am Growth and contractile function of pulmonary arterial smooth muscle cells (P A S M C) and intracellular free Ca 2+ concentration. Results: It was found that N I T significantly inhibited the increase of MTP-induced 5-HT and its receptor-positive cells and the increase of relative content. The number of 5 H T and its receptor positive cells was reduced from (127 494 ± 20 736) / m 2 and (14 624 ± 3 010) / m 2 to (23 814 ± 13 284) / m 2 respectively And (4875 ± 972) / m 2 (P <0.01). 5 H T caused by cultured P A S M C proliferation and contraction have a significant inhibitory effect. This inhibitory effect and its blocking 5 H T Ca2 + influx caused by. CONCLUSION: N I T not only has the function of contracting vasoconstriction and promoting the proliferation of P A S M C, but also inhibits the number of 5 H T-positive cells in the lung tissue of M C T-pulmonary hypertension and 5 H T relative content, which is N I T M C T-one of the important mechanisms of pulmonary hypertension.