【摘要】 目的　研究内源性一氧化碳体系对慢性肺心病肺血管结构重建的调控作用。方法　将36只SD大鼠随机分为正常对照组 (A组 )、4周低O2 高CO2 组 (B组 ) ,4周低O2 高CO+ 2 血晶素组 (C组 ) ,每组 12只。测定各组大鼠肺动脉平均压 (mPAP)、右心室 / (左心室 +室间隔 )重量比 [RV/ (LV +S) ]、肺细小动脉显微和超微结构、血CO浓度、血清及肺组织匀浆上清液血红素氧合酶 1(HO 1)活性和肺细小动脉HO 1及其基因表达的变化。结果　 (1)B组mPAP为 (2 0 1± 0 8)mmHg(1mmHg =0 .133kPa)、RV/ (LV +S)为 (35 5± 1 7) %、与A组 [(15 3± 1 4 )mmHg、(2 6 7± 1 7) % ]及C组[(16 5± 3 7)mmHg、(30 2± 1 6 ) % ]比较差异有显著性 (P均 <0 0 1)。 (2 )B组肺细小动脉血管结构重建的显微形态测定指标与A、C组比较差异也有显著性 (P <0 0 1)。 (3)B组全血CO含量、血清及肺组织匀浆HO 1活性、肺细小动脉HO 1及其mRNA分别为 (2 1± 0 9) %、(73± 18)nmol·L-1·h-1、(175 1± 311)pmol·mg-1·h-1、0 191± 0 0 12和 0 30 1± 0 0 17,与A组 [(0 5± 0 3) %、(2 5± 8)nmol·L-1·h-1、(385± 4 6 )pmol·mg-1·h-1、0 0 5 9± 0 0 0 5、0 131± 0 0 11]和C组 [(4 9± 2 1) %、(132±39)nmol·L-1·h-1更多还原

【Abstract】 Objective To study the effect of carbon monoxide on pulmonary vessel remodeling of chronic pulmonary heart disease Methods Thirty six sprague dawley rats were randomly divided into three groups: control group, and hypoxic hypercapnic group,and hypoxic hypercapnia + hemin group Blood CO concentration (COHb%), activity of HO 1 in blood serum and lung homogenate, pulmonary arteriole micromorphometric index, HO 1 and HO 1 mRNA were measured Results (1) mPAP and RV/(LV+S) were (20 1±0 8) mm Hg and (35 5±1 7)% in hypoxic hypercapnic group, they were significantly higher than those of control group′s (15 3±1 4) mm Hg,(26 7±1 7)%, and those of hypoxic hypercapnia + hemin (activator of HO 1) group′s (16 5±3 7) mm Hg,(30 2±1 6)% ( P <0 01) (2) Pulmonary arteriole micromorphometric index in rats of hypoxic hypercapnic group were significantly higher than those of control group and hypoxic hypercapnia + hemin group ( P <0 01) (3) Blood CO concentration, activity of HO 1 in blood serum and lung homogenate, content of HO 1 and HO 1 mRNA in pulmonary arterioles in rats of hypoxic hypercapnic group were (2 1±0 9)%, (73±18) nmol·L -1 ·h -1 , (1 751±311) pmol·mg -1 ·h -1 , 0 191±0 012 and 0 301±0 017, were significantly higher than those of control group: (0 5±0 3)%, (25±8) nmol·L -1 ·h -1 , (385±46) pmol·mg -1 ·h -1 , 0 059±0 005, 0 131±0 011, but were significantly lower than those of hypoxic hypercapnia + hemin group: (4 9±2 1)%, (132±39) nmol·L -1 ·h -1 , (2 849±426) pmol·mg -1 ·h -1 , 0 272±0 013, 0 339±0 020 ( P <0 01) (4) Correlation analysis revealed that the relationship between carbon monoxide system and pulmonary arteriole micromorphometric index was significantly negative ( P <0 01) Conclusion Up regulation of endogenous carbon monoxide system can inhibit pulmonary vessel remodeling in rats with chronic pulmonary heart disease induced by hypoxia and hypercapnia更多还原