【摘要】 目的　研究肺出血幼兔肺动脉压力及肺血管内皮细胞超微结构的变化 ,为预防新生儿肺出血提供理论依据。方法　 15只幼兔耳缘静脉注射高分子右旋糖苷 (T 5 0 0 ) 1ml/kg,连续 5d (7只 )和 8d (8只 )。对照组 (8只 )注射相同剂量的生理盐水 ,连续 5d。经右心室穿刺 ,通过多道生理记录仪记录右心室压力 ,并以此反映肺动脉压力。透射电镜观察肺血管内皮细胞超微结构变化。结果　实验组幼兔右心收缩压第 5天为 (16 6± 1 2 )mmHg (1mmHg =0 .133kPa) ,第 8天为 (19 2±1 1)mmHg ,明显高于对照组的 (12 2± 1.3)mmHg(P <0 .0 1)。超微结构表现为肺动脉内皮细胞水肿 ,肺泡毛细血管内皮细胞破坏 ,II型上皮细胞内层状小体空泡变性。结论　高粘滞血症引起幼兔肺出血 ,伴有肺动脉压力显著升高及肺毛细血管内皮细胞和肺泡上皮细胞超微结构异常。这些改变是高粘滞血症导致幼兔发生肺出血的病理基础。更多还原

【Abstract】 Objective To observe the pulmonary artery pressure and pulmonary endothelium ultrastructure in immature rabbits with pulmonary hemorrhage. Methods Twenty three immature Japan white rabbits aged 20 days to 30 days and weighing 310 g to 370 g were randomly divided into 2 groups. The first group as controls ( n =8) received a dose of 1 ml/kg of normal saline for 5 days; the second group ( n =15) as experimental group received a dose of 1 ml/kg of dextran (10%, T 500) intravenously for 5 days (7/15) and 8 days (8/15), respectively. The right ventricular pressures were measured by polygraph system for recording pulmonary artery pressures. Lungs were removed and fixed for examinations of transmission electron microscopy after rabbits were killed.Results Rabbits in experimental group developed higher right ventricular pressures, (16.6±1.2) mm Hg (1 mm Hg=0.133 kPa) ( n =7) in the 5th day and (19±1.1) mm Hg ( n =8) in the 8th day which were higher significantly than those in control group (12.2±1.3) mm Hg ( F =77.9, P <0.01). The ultrastructure study revealed disruptions of the capillary endothelial and alveolar epithelial (mainly in epithelial II) cells. Red blood cells were seen in the alveolar spaces as well as in the interstitum. Conclusion The blood hyperviscosity could induce the pulmonary hemorrhage in immature rabbits,and company with pulmonary hypertension and ultrastructural disruptions in pulmonary endothelium and epithelium.更多还原