摘要
目的:观察CCl4诱导的肝硬化模型中,CO及肺泡血管壁通透性的变化.方法:CCl4皮下注射制备大鼠肝硬化模型,动脉插管生理多导仪记录心率、平均动脉压的变化,门静脉插管测定门静脉压力,血浆CO水平的测定用联二亚硫酸盐还原法,静脉注射伊文思蓝测定肺泡血管壁通透性.结果:CCl4成功复制肝硬化模型,显微镜下见正常肝小叶被完全破坏,有典型的假小叶形成.肺组织肺泡壁增厚,肺毛细血管管腔扩张,部分肺泡腔变小.与正常对照组相比,肝硬化组平均动脉压显著降低(15.92kPa±0.74kPavs18.93kPa±0.71kPa,P<0.01),门脉压力显著增高(16.67cmH2O±0.63cmH2Ovs8.82cmH2O±0.29cmH2O,P<0.01);血浆CO水平显著升高(18.69μmol/L±1.86μmol/Lvs10.27μmol/L±1.21μmol/L,P<0.01);肺组织EB含量明显增加(36.57μg/g±1.69μg/gvs29.83μg/g±2.34μg/g,P<0.01).结论:HO-CO的激活、肺泡血管壁通透性增加可能是肝肺综合征的重要原因.
AIM: To examine possible alterations in plasma carbon monoxide (CO) levels and alveolar permeability in rats with carbon tetrachloride- induced cirrhosis. METHODS: Liver cirrhosis was induced in rats by subcutaneous administration of carbon tet- rachloride. Mean arterial pressure (MAP, kPa), heart rate (HR, b/min), and portal pressure (PP, cm/H2O) were monitored by using an indwelling catheter. Plasma CO levels were determined by Chalmers method, and alveolar permeability was measured using the Evens blue extravasation technique. RESULTS: Typical features of cirrhosis were histologically observed in carbon tetrachloridetreated rats. Compared with normal control rats, cirrhotic rats presented a significant increase in portal pressure (16.67 cmH2O ± 0.63 cmH2O vs 8.82 cmH2O ± 0.29 cmH2O; P 〈 0.01), plasma CO levels (18.69 μmol/L ± 1.86 μmol/L vs 10.27 μmol/L ± 1.21 μmol/L; P 〈 0.01), and Evens blue extravasation (36.57 μg/g ± 1.69 μg/g vs 29.83 μg/g ± 2.34 μg/g; P 〈 0.01), but a significant decrease in mean arterial pressure (15.92 kPa ± 0.74 kPa vs 18.93 kPa ± 0.71 kPa; P 〈 0.01). CONCLUSION: Activation of the HO-CO system and increased alveolar permeability may be important causes of development of hepatopulmonary syndrome in patients with cirrhosis.
出处
《世界华人消化杂志》
CAS
北大核心
2011年第3期281-283,共3页
World Chinese Journal of Digestology
关键词
肝硬化
肝肺综合征
一氧化碳
肺泡通透性
Cirrhosis
Hepatopulmonary syndrome
Carbon monoxide
Alveolar permeability