论文部分内容阅读
目的研究新型气体信号分子硫化氢(H2S)在大鼠低氧性肺动脉高压形成中对一氧化碳(CO)/血红素加氧酶(HO1)体系的调节作用,以深入探讨H2S在大鼠低氧性肺动脉高压形成中的病理生理意义。方法将27只大鼠随机分为4组对照组(7只),低氧组(7只),低氧+硫氢化钠(NaHS)组(7只),低氧+炔丙基甘氨酸(PPG)组(6只)。低氧21d后分别测定肺动脉平均压、血浆H2S及CO含量,观察肺动脉平滑肌HO1蛋白及HO1mRNA表达。结果随着低氧性肺动脉高压的形成,血浆H2S的含量显著下降,低氧组[(196±22)μmol/L]与对照组[(294±26)μmol/L]比较差异有显著性(P<005);而CO含量、大、中、小各级肺动脉平滑肌HO1蛋白表达[对照组、低氧组分别为(0313±0020)μmol/L、(0348±0021)μmol/L,066±008、079±008,064±005、077±008,054±005、076±009]及其mRNA表达(对照组、低氧组分别为0573±0148、0813±0052,0532±0131、0831±0043,0473±0102、0819±0032)显著升高(P均<005);外源性给予H2S的供体后,低氧+NaHS组血浆H2S含量[(324±33)μmol/L]显著高于低氧组[(196±22)μmol/L,P<005],肺动脉压显著下降(P<005),且血浆CO含量[(0393±0032)μmol/L]、大、中、小各级肺动脉平滑肌HO1蛋白表达(088±004、089±005、089±006)及mRNA表达(0913±0022、0
Objective To study the regulatory effect of a novel gas signaling molecule hydrogen sulfide (H2S) on carbon monoxide (CO) / heme oxygenase (HO1) system in hypoxic pulmonary hypertension in rats. Pathophysiological Significance in the Formation of Pulmonary Hypertension. Methods Twenty-seven rats were randomly divided into four groups: control group (7 mice), hypoxia group (7 mice), hypoxia + NaHS group (7 mice), hypoxia + propargylglycine ) Group (6). After 21 days of hypoxia, mean pulmonary artery pressure, plasma H2S and CO contents were measured, and HO1 protein and HO1 mRNA expression in pulmonary artery smooth muscle cells were observed. Results Compared with control group [(294 ± 26) μmol / L], the level of plasma H2S was significantly decreased in hypoxia group [(196 ± 22) μmol / L] P <0.01). However, the content of CO, HO1 protein in pulmonary artery smooth muscle of rats in the control group and the hypoxia group were (0313 ± 0020) μmol / L, (0348 ± 0021) μmol / L, 008,079 ± 008,064 ± 005,077 ± 008,054 ± 005,076 ± 009] and its mRNA expression (control group, hypoxia group were 0573 ± 0148,0813 ± 0052,0532 ± 0131,0831 ± 0043,0473 ± 0102 , Respectively (P <0.05). The levels of H2S in the hypoxia + NaHS group [(324 ± 33) μmol / L] were significantly higher than those in the hypoxia group [ (196 ± 22) μmol / L, P <005], pulmonary arterial pressure decreased significantly (P <005), and the content of CO in plasma [(0393 ± 0032) μmol / L] Expression (088 ± 004, 089 ± 005, 089 ± 006) and mRNA expression (0913 ± 0022,