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目的用药物法建立犬肺动脉高压模型。方法野百合碱经脱氢处理成脱氢野百合碱 (dehydromonocrotaline,DMCT),经心导管注射入犬右心房,于注射药物后4周、8周测定肺动脉压力等血液动力学参数,并行肺组织病理检查,评估周围肺肌性动脉肌化情况、肌性肺动脉中膜肥厚程度。结果 DMCT(3 mg／kg)组8只犬存活2只,DMCT(2 mg／kg)组8只犬与对照组犬均存活。DMCT组4周后平均肺动脉压(mMPAP)(20．7±3．1)mm Hg(1 mm Hg=0．133 kPa),8周后mPAP(30．2±2．6)mm Hg,肺动脉收缩压(sPAP)和肺动脉楔压(PCWP)亦升高,与给药前相比,差异有统计学意义(P<0．01)。DMCT组8周后 mPAP、sPAP与PCWP亦明显高于溶剂对照组,差异有统计学意义,P<0．01。8周后DMCT组直径为15- 50μm的肺肌性动脉肌化数(54．3±6．6)％,直径为100-200μm的肺肌性动脉的中膜厚度百分比(27．3± 5．7)％,均高于溶剂对照组,差异有统计学意义(P<0．01),右心肥大指数增加(P<0．05)。光学显微镜下观察到DMCT组肺泡区肺肌性动脉中膜肥厚,新生内膜形成,管腔变小。结论 DMCT可成功诱导犬肺动脉高压模型,模拟人类终末期肺高压的病理特点。
Objective To establish a model of canine pulmonary hypertension with drug therapy. METHODS: Hornylline was dehydrated to dehydromonocrotaline (DMCT) and injected into the right atrium of the dog through a cardiac catheter. The hemodynamic parameters such as pulmonary arterial pressure were measured at 4 weeks and 8 weeks after drug injection. The lung tissues Pathological examination to assess the surrounding muscular pulmonary artery muscular condition, muscular pulmonary artery membrane hypertrophy. Results Eight dogs in DMCT (3 mg / kg) group survived 2 dogs and 8 dogs in DMCT (2 mg / kg) group survived. In the DMCT group, mean pulmonary arterial pressure (mPAP) (20.7 ± 3.1) mm Hg (1 mm Hg = 0.133 kPa), mPAP (30.2 ± 2.6) mm Hg after 8 weeks, pulmonary artery Systolic blood pressure (sPAP) and pulmonary artery wedge pressure (PCWP) also increased, compared with pre-administration, the difference was statistically significant (P <0.01). The levels of mPAP, sPAP and PCWP in DMCT group were significantly higher than those in solvent control group after 8 weeks, P <0.01. After 8 weeks, the number of muscular pulmonary artery in DMCT group (15-50 μm) .3 ± 6.6)%, while the percentage of tunica media in the diameter range of 100-200 μm was (27.3 ± 5.7)%, which was higher than that in the solvent control group (P < 0.01), right heart hypertrophy index increased (P <0.05). Under the light microscope, the mediastinal hypertrophy and pulmonary neovascularization in the pulmonary alveolar area were observed in the DMCT group, and the lumen became smaller. Conclusion DMCT can successfully induce canine pulmonary hypertension model to simulate the pathological features of human end-stage pulmonary hypertension.