摘要
目的 :探讨外源性低浓度一氧化碳 (CO)在低氧性肺动脉高压中的作用。方法 :6 0只Wistar大鼠随机分为常氧组、低氧组、血晶素组、锡原卟啉组和低浓度CO组 ,每组 12只。处理完毕后 ,右心导管法测定肺动脉平均收缩压和右心室压。杀鼠取肺组织 ,应用分光光度法测定肺组织HO - 1活性 ,并进行常规免疫组织化学染色 ,应用逆转录多聚酶链式反应测定测定肺组织的HOmRNA水平。结果 :①低浓度CO组肺动脉压为(18 5 2± 3 2 4)mmHg ,明显低于低氧组但仍高于常氧组 (均为P <0 0 1) ;②低浓度CO组HO - 1活性为(10 5 2 48± 30 8 49)nmol·g-1(protein) ,显著高于正常组 (P <0 0 1) ;③低浓度CO组HO - 1蛋白表达水平均高于常氧组和低氧组 (P <0 0 1) ;④低浓度CO组HO - 1mRNA水平的光密度值为 2 6 3± 0 18,显著高于正常组 (P<0 0 1)。结论 :CO -HO系统参与了低氧性肺动脉高压的发病机制 ;低浓度CO可以有效促进HO - 1mRNA表达 ,使HO - 1活性和蛋白表达水平升高 ,进而部分降低肺动脉压力。
AIM: To explore the effect of exogenous carbon monoxide (CO) on the hypoxic pulmonary arterial hypertension in the rat. METHODS: 60 rats were randomly divided into 5 groups: Normal group\, hypoxic group\, Hermin group\, Znpp group and CO group. HO-1 activity was examined by spectrophotometer and lung tissues was stained by immunohistochemical method. HO-1 mRNA level was tested by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: (1) The pulmonary arterial pressure (18.52±3.24 mmHg) in CO group was higher than anoxic group and lower than hypoxic group (P<0.01); (2) The HO-1 activity in CO group was markedly increased compared with Normal and Hypoxic group. (3) The level of HO-1 protein and HO-1 mRNA were obviously promoted in CO group compared with Normal and Hypoxic group.CONCLUSION: CO-HO system was involved in the hypoxic pulmonary arterial hypertension.CO in low density may induce HO-1 mRNA expression, promote HO-1 acitvity and HO-1 protein level, and result in partly decreasing the pulmonary arteral pressure.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第11期1178-1181,I003,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金!(No .3970 0 0 5 7)
全军"九五"医药卫生科研基金! (No .98M0 77)
