Effects of exogenous hydrogen sulfide on pulmonary hypertension  in rabbits with endotoxic shock

doi:10.12047/j.cjap.6277.2022.050

Abstract

Abstract: Objective: To investigate the effects of exogenous hydrogen sulfide (H₂S) on pulmonary vascular reactivity induced by endotoxic shock (ES) in rabbits. Methods: In this experiment, the model of endotoxic shock (ES) was induced by injection of lipopolysaccharides (LPS) to New Zealand big eared white rabbit through jugular vein (8 mg/0.8 ml/kg), the intervention was performed by H₂S donor(sodium hydrosulfide, NaHS) which was injected intraperitoneally (28 μmol/kg) 15 min in advance. New Zealand rabbits were randomly divided into 4 groups(n=8):control group, LPS group, LPS+NaHS group and NaHS group. The changes of mean arterial pressure (MAP) and mean pulmonary arterial pressure (MPAP) were detected. The tension of pulmonary artery ring (PARs) was detected byin vitro vascular ring technique. The ultrastructure of pulmonary artery wall and pulmonary artery endothelial cells were observed by light microscope and scanning electron microscope. Results: ①MAP was decreased while MPAP was increased in rabbits after LPS injection, and ES animal model was established successfully. Compared with LPS group, mPAP of rabbit in LPS+NaHS group was decreased significantly (all P＜0.05). ②Compared with normal control group, pulmonary artery of rabbits in LPS group had an increased contractile response to phenylephrine (PE) and a decreased relaxation response to acetylcholine (ACh) (both P＜0.01); Compared with LPS group, pulmonary artery of rabbits in LPS+NaHS group had a decreased contractile response to PE and an increased relaxation response to ACh (both P＜0.05). ③Under light microscope, the structure of vascular endothelial cells was continuous in the normal control group, the elastic fibers were intact in the subcutaneous layer, and the smooth muscle layer was arranged neatly. LPS can shed some of the pulmonary artery endothelial cells, break the subcutaneous elastic fibers, and disorder the smooth muscle layer structure. Compared with LPS group, the injury of pulmonary artery wall in LPS+NaHS group was ameliorated. The morphology of pulmonary artery wall was normal in NaHS group. It is showed that some endothelial cells of pulmonary artery were missing in LPS group by Scanning electron microscopy. The morphology of pulmonary artery endothelial cells in LPS+NaHS group was similar to that in the control group: slightly widened intercellular space was observed, and no cell exfoliation was observed. Conclusion: These results suggest that exogenous H₂S can protect pulmonary artery endothelial cells and regulate the reactivity changes of pulmonary artery during ES, which may be one of the mechanisms reducing PAH in ES rabbits.

Key words: hydrogen sulfide, lipopolysaccharides, shock, pulmonary artery, rabbit

CLC Number:

R363.2

GUO Zan, LIU Yi-xian, QI Jie, XIAN Xiao-hui, HUANG Xin-li. Effects of exogenous hydrogen sulfide on pulmonary hypertension in rabbits with endotoxic shock[J]. CJAP, 2022, 38(3): 264-269.

References

[1] Toney BM, Fisher AJ, Albrecht M, et al. Selective endothelin-A receptor blockade attenuates endotoxin-induced pulmonary hypertension and pulmonary vascular dysfunction[J]. Pulm Circ, 2014, 4(2) : 300-310.
[2] Rui W. Two's company, three's a crowd: Can H₂S be the third endogenous gaseous transmitter? [J]. FASEB J, 2002, 16(13): 1792-1798.
[3] 黄新莉, 周晓红, 韦鹏, 等. 内源性硫化氢在脂多糖引起的肺动脉高压中的作用[J]. 生理学报, 2008, 60(2): 211-215.
[4] Chen J, Zhang H, Yu W, et al. Expression of pulmonary arterial elastin in rats with hypoxic pulmonary hypertension using H₂S[J]. J Recept Signal Transduct Res, 2020, 40(4): 383-387.
[5] Fernández RA, Soriano RN, Francescato HD, et al. Cryogenic role of central endogenous hydrogen sulfide in the rat model of endotoxic shock[J]. Brain Res, 2016, 1650: 218-223.
[6] 赵美平, 缪初蕾, 张聪聪, 等. 川芎嗪注射液对慢性阻塞性肺疾病患者肺动脉高压的作用及其机制[J]. 中国应用生理学杂志, 2016, 32(5): 406-412.
[7] Turzo M, Spöhr FA, Felix L, et al. Kv7 channel inhibition increases hypoxic pulmonary vasoconstriction in endotoxemic mouse lungs[J]. Exp Lung Res, 2020, 46(10): 363-375.
[8] 段国辰, 凌亦凌, 谷振勇, 等. 八肽胆囊收缩素对家兔内毒素休克时肺动脉张力的影响[J]. 生理学报, 2003, 55(2): 201-205.
[9] Lin SL, Lee YM, Chang HY, et al. Effects of naltrexone on lipopolysaccharide-induced sepsis in rats[J]. J Biomed Sci, 2005, 12(2): 431-440.
[10] Li DK, Mao JY, Long Y, et al. Pulmonary hypertension with adult respiratory distress syndrome: prevalence, clinical impact, and association with central venous pressure[J]. Pulm Circ, 2020, 10(3): 2045894020933087.
[11] Yin TJ, Hu YS, Cheng S, et al. Dynamic changes of pulmonary arterial pressure in perinatal neonates with pulmonary and extrapulmonary acute lung injury/respiratory distress syndrome[J]. Medicine (Baltimore), 2019, 98(11): e14830
[12] Zhang H, Lin Y, Ma Y, et al. Protective effect of hydrogen sulfide on monocrotaline-induced pulmonary arterial hypertension via inhibition of the endothelial mesenchymal transition[J]. Int J Mol Med, 2019, 44(6): 2091-2102.
[13] Li M, Mao J, Zhu Y. New therapeutic approaches using hydrogen sulfide donors in inflammation and immune response[J]. Antioxid Redox Signal, 2021, 35(5): 341-356.
[14] Kshirsagar V, Thingore C, Gursahani M, et al. Hydrogen sulfide ameliorates Lipopolysaccharide-induced memory impairment in mice by reducing apoptosis, oxidative, and inflammatory effects[J]. Neurotox Res, 2021, 39(4): 1310-1322.
[15] 杨锐, 贾强, 刘小粉, 等. 硫化氢对大鼠糖尿病心肌病氧化应激及内质网应激的影响[J]. 中国应用生理学杂志, 2016, 32(1): 8-12.
[16] Zhang H, Hao LZ, Pan JA, et al. Microfluidic fabrication of inhalable large porous microspheres loaded with H₂S-releasing aspirin derivative for pulmonary arterial hypertension therapy[J]. J Control Release, 2021, 329: 286-298.
[17] 翟羽, 周晓红, 刘会, 等. 饱和氢气生理盐水对盲肠结扎穿孔大鼠肺损伤的干预作用[J]. 中国应用生理学杂志, 2019, 35(2): 107-113.
[18] Abdelrahman RS, El-Awady MS, Nader MA, et al. Hydrogen sulfide ameliorates cardiovascular dysfunction induced by cecal ligation and puncture in rats[J]. Hum Exp Toxicol, 2015, 34(10): 953-964.
[19] Hui Y, Du J, Tang C, et al. Changes in arterial hydrogen sulfide (H(2)S) content during septic shock and endotoxin shock in rats[J]. J Infect, 2003, 47(2): 155-160.
[20] Ahmad A, Druzhyna N, Szabo C. Delayed treatment with sodium hydrosulfide improves regional blood flow and alleviates cecal ligation and puncture (CLP)-induced septic shock[J]. Shock, 2016, 46(2): 183-193.

Effects of exogenous hydrogen sulfide on pulmonary hypertension in rabbits with endotoxic shock

PDF (PC)

Knowledge

Abstract

Cite this article

share this article

References

Related Articles 15

Recommended Articles

Metrics

Comments

[1]	CHEN Chang-gui, HE Li-qun, TIAN Li-qun, YI Chun-feng. Effects of GW501516 on the proliferation of pulmonary artery smooth muscle cells induced by hypoxia and its mechanisms [J]. CJAP, 2022, 38(2): 119-125.
[2]	XI Yu-xin, WEN Xin, JIAO Li-jie, WEI Ya-xin, CHANG Gui-quan, WU Ren, SUN Feng-qi, HAO Jing-hui, LI Hong-zhu. Effects of exogenous H₂S on hepatic fibrosis in diabetic mice and its mechanism [J]. CJAP, 2020, 36(4): 318-320.
[3]	ZHOU Bi-ye, LI Jing, LI Ming-gao, SUN Hai-wen, ZHOU Jia-xing, HAN Lei. Effect of repeated horizontal acceleration exposure on cardiac structure in New Zealand rabbits [J]. CJAP, 2020, 36(2): 134-137.
[4]	BU Bao-ying, XU Xi-yuan, HAN Jun-ping, YANG Jing-ping. Effects of hypoxia on the expression of HMGB1 and related inflammatory factors in human pulmonary artery smooth muscle and pulmonary artery endothelial cells [J]. CJAP, 2019, 35(5): 406-409.
[5]	ZHAI Yu, ZHOU Xiao-hong, LIU Hui, FU Hong-yi, FAN Ya-min, HUANG Xin-li. The interventional effects of saturated hydrogen saline on lung injury in rats with cecal ligation and puncture operation [J]. CJAP, 2019, 35(2): 107-112.
[6]	JIA Qiang, WANG Lei, WANG Qi-yi, LIU Xiao-fen, MA Shan-feng, YANG Rui. Effects of hydrogen sulfide on renal fibrosis in diabetic rats and its mechanism [J]. CJAP, 2018, 34(6): 572-576.
[7]	JIANG Feng-qi, YUAN Ying, XIANG Zuo-jun, HUANG Pan-rui, WU He, WANG Shi-qi, WANG Juan, PENG Hui, LUO Hai. Effects of chloride channels on hemolysis induced by puerarin injection [J]. CJAP, 2018, 34(5): 441-444.
[8]	SUN Wei-ming, ZHANG Yuan-zhou, WEN Xin, XI Yu-xin, YUAN Di, WANG Yue-hong, WEI Can, XU Chang-qing, LI Hong-zhu. Protective effects of exogenous H₂S to the recovery of hypoxia post-conditioning on aged H9C2 cells and the underling mechanisms [J]. CJAP, 2018, 34(4): 289-293.
[9]	ZHANG Jing-jing, CHEN Jun-hao, ZHAO Mei-ping, WU Yuan-ling, ZHANG Cong-cong, YING Lei, CHEN Xi-wen, WANG Wan-tie. The role of endoplasmic reticulum stress in pulmonary hypertension in rat induced by chronic hypoxia and hypercapnia [J]. CJAP, 2018, 34(4): 327-333.
[10]	ZHOU Ben-mei, GUO Xing-ming, ZHENG Yi-neng, LI Hong-quan. Changes of some biochemical markers and cardiac function in New Zealand rabbits with chronic heart failure [J]. CJAP, 2018, 34(1): 74-77.
[11]	MA Jie, GUO Kang, LV Lin-ya, LI Xin-juan, WANG Lu, WEI Lin-yu, ZHAO Hong-gang, LI Dong-liang. Effect of NaHS on ATP-induced P2X receptor expression in rat microglia [J]. CJAP, 2017, 33(6): 519-523.
[12]	YANG Rui, JIA Qiang, MA Shan-feng, LIU Xiao-fen, GAO Qin, WANG Lei. Effects of hydrogen sulfide on NO content and iNOS activity in diaphragm from type 1 diabetic rats [J]. CJAP, 2017, 33(3): 248-251.
[13]	WANG Zi-jian, LIU Jun-fen, JIANG Li-na, ZHANG Li-min, LIU Gui-qing, WANG Huai-huai, ZHAO Zi-gang, NIU Chun-yu. Role of mesenteric lymph drainage in the balance of ACE/ACE2 in murine myocardium following hemorrhagic shock [J]. CJAP, 2017, 33(1): 61-65.
[14]	WANG Dan-dan, WANG Yu, WANG Jing-jing, CHEN Ying, YE Zheng, LI Jing, LI Min, ZHU Zai-man, PAN Qun-wan. The changes of electric shock avoidance response and local field potentials on hippocampal CA3 region of the adolescent rats with high fat feeding [J]. CJAP, 2016, 32(6): 545-549.
[15]	JIANG Wei, ZHANG Xian, ZHOU Ai-Ling. The role of TLR₄/P38/JNK signaling pathway in apoptosis of hippocampal neurons [J]. CJAP, 2016, 32(6): 571-576.