Related Experiment Video
Updated: Dec 26, 2025

Shunt Surgery, Right Heart Catheterization, and Vascular Morphometry in a Rat Model for Flow-induced Pulmonary Arterial Hypertension
Published on: February 11, 2017
Expression of pulmonary arterial elastin in rats with hypoxic pulmonary hypertension using H2S
Juan Chen1, Haizhou Zhang2, Wancheng Yu2
1Department of gynaecology and obstetrics, Jinan No.1 people's Hospital, Jinan, People's Republic of China.
Abstract:
Object: This study analyses the changes of pulmonary arterial elastin expression inhibited by hydrogen sulfide (H2S) in rats with hypoxic pulmonary hypertension.Method: The research used 30 healthy rats and randomly divided them into control group, hypoxia group, and hypoxia + sodium hydrosulfide group. Each group contains 10 samples. The right catheterization was selected to measure the mean pulmonary artery pressure (mPAP). The RV/LV + S ratio was calculated through separating the right ventricle and the left ventricle plus the interventricular septum. Optical microscopy was used to observe the changes of pulmonary vascular structure. The research used immunohistochemistry to express the levels of elastin and transforming growth factor beta (TGF-β).Results: The ratios of Mpap and RV/LV + S in the hypoxic group exceed the control group. The hypoxia + sodium hydrosulfide group (hypoxia + NaHS) is lower than the hypoxic group. In the hypoxic group, the elastic expressions of medium and small pulmonary artery smooth muscle cells exceed the control group. The expression of elastin in hypoxic + NaHS medium and small pulmonary artery smooth muscle cells is lower than that of the control group.The protein expression levels of α-SM-actin in muscle arterial smooth muscle of pulmonary arterioles in hypoxic group, control group and hypoxic + NaHS group were 49.84% + 6.27%, 56.84% + 6.38%, 23.82% + 3.84%, 27.51% + 3.24%, 29.00% + 4.05%, 34.72% + 3.38%.Conclusion: Hydrogen sulfide in rats with hypoxic pulmonary hypertension can inhibit the expression of elastin in its extracellular matrix, which also has remarkable regulation function in forming HPH and remodeling hypoxic pulmonary vascular structure.

