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用野百合碱（ＭＣＴ）复制大鼠慢性肺动脉高压（ＰＨ）病理模型，探讨钙拮抗剂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）对ＰＨ的防治作用．ＤＣＤＤＰ５，５０，５００μｇ·ｋｇ－１ｉｐ，每日１次，连续２８ｄ；ＭＣＴ６０ｍｇ·ｋｇ－１在第１次给ＤＣＤＤＰ后３０ｍｉｎｓｃ．观察肺血流动力学指标变化，血浆和肺匀浆中内皮素样免疫反应物（ｉｒ－ＥＴ），一氧化氮（ＮＯ）含量，超氧化物歧化酶（ＳＯＤ）活性和丙二醛（ＭＤＡ）含量的改变．三种不同剂量的ＤＣＤＤＰ分别使平均肺动脉压从４．５±０．９ｋＰａ（ＭＣＴ组）降至３．２±０．２，３．５±０．６和３．８±０．９ｋＰａ，肺血管阻力从１１８±１７ｋＰａ·ｍｉｎ－１·Ｌ－１（ＭＣＴ组）降至６５±１６，６８±１８和７６±１８ｋＰａ·ｍｉｎ－１·Ｌ－１（Ｐ＜０．０１），提示在本实验剂量范围内，中，低剂量ＤＣＤＤＰ防治效果似较好．ＤＣＤＤＰ不影响ＭＣＴ性ＰＨ时血浆和肺匀浆中ｉｒ－ＥＴ的改变，但可显著升高肺匀浆中ＮＯ的含量和ＳＯＤ活性，使肺匀浆中ＭＤＡ含量降至正常，这可能是其降低肺动脉压的机理之一．
Chronic pulmonary hypertension (PH) pathological model was duplicated with monocrotaline (MCT) and the effects of calcium antagonist 2,6-dimethyl-4- (2-chlorophenyl) -1,4-dihydro- Preventive effect of 5-pyridinedicarboxylate (DCDDP) on PH. DCDDP5,50,500μg · kg-1ip, once a day for 28 days; MCT60mg · kg-1 after the first DCDP to 30minsc. The changes of pulmonary hemodynamic indexes, the contents of endothelin-like immunoreactive substance (IR-ET), nitric oxide (NO), superoxide dismutase (SOD) ) Content changes. Three different doses of DCDDP decreased mean pulmonary arterial pressure from 4.5 ± 0.9 kPa (MCT group) to 3.2 ± 0.2, 3.5 ± 0.6 and 3.8 ± 0.9 kPa, respectively Vascular resistance decreased from 118 ± 17 kPa · min-1 · L-1 (MCT group) to 65 ± 16,68 ± 18 and 76 ± 18 kPa · min-1 · L-1 (P <0.01) In the experimental dose range, medium and low doses of DCDDP control effect seems better. DCDDP did not affect the changes of ir-ET in plasma and lung homogenate when MCT PH, but could significantly increase NO content and SOD activity in lung homogenate, and the content of MDA in lung homogenate decreased to normal, which may be due to One of the mechanisms of lowering pulmonary arterial pressure.