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[高肺血流诱导大鼠肺动脉高压早期内源性硫化氢通路的动态变化]

[The dynamic changes in endogenous hydrogen sulfide pathway at the early stage of pulmonary hypertension induced by high pulmonary flow in rats].

作者信息

Li Xiao-Hui, Bu Ding-Fang, Jin Hong-Fang, Ding Ya-Guang, Du Jun-Bao, Li Jian, Tang Chao-Shu

机构信息

Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Feb;23(1):75-9.

Abstract

AIM

To explore the time-dependent changes of endogenous hydrogen sulfide system at the early stage of pulmonary hypertension induced by high pulmonary flow in rats.

METHODS

Eighty male SD rats, whose weight ranged 140 - 160 g, were randomly divided into control group (n = 40) and shunt group (n = 40). Rats in shunt group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. After 1 d, 3 d, 1 week, 4 week and 8 weeks of experiment, systolic pulmonary artery pressure (SPAP) of each rat, the H2S of rat lung tissue and CSEmRNA of rat lung tissue were evaluated, respectively.

RESULTS

SPAP increased significantly as compared with those in control group in 1 week and 8 weeks of experiment. In contrast to control group, the H2S of rat lung tissue increased significantly on 3 d and in 4 weeks, respectively. Meanwhile, in contrast to control group, relative amount of CSE mRNA of lung tissues elevated significantly on 3 d and in 4 weeks, respectively. Moreover, SPAP and the H2S of rat lung tissue, the CSE mRNA of rat lung tissue correlated negatively in 1 week, 4 weeks and 8 weeks of experiment.

CONCLUSION

Animal model of rats with high pulmonary blood flow exhibited pulmonary hypertension. Lung tissue H2S and CSE mRNA of rats exhibited double peaks within 8 weeks. These results revealed that endogenous H2S system might be relevant with the development of pulmonary hypertension induced by high pulmonary blood flow, and probably, it played a protective role in the regulation of pulmonary hypertension, especially, at its early stage.

摘要

目的

探讨大鼠高肺血流量诱导的肺动脉高压早期内源性硫化氢系统的时间依赖性变化。

方法

80只体重在140 - 160 g之间的雄性SD大鼠随机分为对照组(n = 40)和分流组(n = 40)。分流组大鼠行腹主动脉-下腔静脉分流术以建立高肺血流量动物模型。实验1天、3天、1周、4周和8周后,分别评估每只大鼠的收缩期肺动脉压(SPAP)、大鼠肺组织硫化氢含量及大鼠肺组织CSEmRNA水平。

结果

实验1周和8周时,与对照组相比,SPAP显著升高。与对照组相比,大鼠肺组织硫化氢含量分别在3天和4周时显著升高。同时,与对照组相比,肺组织CSE mRNA相对含量分别在3天和4周时显著升高。此外,实验1周、4周和8周时,SPAP与大鼠肺组织硫化氢含量、肺组织CSE mRNA呈负相关。

结论

高肺血流量大鼠动物模型出现肺动脉高压。大鼠肺组织硫化氢和CSE mRNA在8周内呈现双峰变化。这些结果表明内源性硫化氢系统可能与高肺血流量诱导的肺动脉高压的发生发展有关,并可能在肺动脉高压的调节中发挥保护作用,尤其是在其早期阶段。

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