Role of endogenous hydrogen sulfide in pulmonary hypertension induced by lipopolysaccharide.
- Author:
Xin-Li HUANG
1
;
Xiao-Hong ZHOU
;
Peng WEI
;
Xiao-Jing ZHANG
;
Xiang-Yan MENG
;
Xiao-Hui XIAN
Author Information
1. Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China. huangxinli2006@hotmail.com
- Publication Type:Journal Article
- MeSH:
Animals;
Arterial Pressure;
Cystathionine gamma-Lyase;
metabolism;
Hydrogen Sulfide;
metabolism;
Hypertension, Pulmonary;
chemically induced;
metabolism;
Lipopolysaccharides;
adverse effects;
Male;
Rats;
Rats, Sprague-Dawley;
Sulfides;
pharmacology
- From:
Acta Physiologica Sinica
2008;60(2):211-215
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of the present study was to explore the role of endogenous hydrogen sulfide (H2S) in pulmonary arterial hypertension induced by endotoxin. Adult male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group (0.5 mL/kg body weight of normal saline, i.v.), lipopolysaccharide (LPS)-treated group (5 mg/kg body weight of LPS, i.v.), LPS + NaHS (5 mg/kg body weight of LPS, i.v., and 28 μmol/kg body weight of NaHS, i.p.) and LPS + PPG group (5 mg/kg body weight of LPS, i.v., and 30 μmol/kg body weight of PPG, i.p.). Rats were anesthetized with 20% urethane (1 g/kg body weight, i.p.). A polyethylene catheter was inserted into the pulmonary artery through the right external jugular vein to measure the mean pulmonary arterial pressure (mPAP) for 7 h, and then the pulmonary artery was isolated rapidly by the method described previously. Pulmonary arterial activity was detected. H2S concentration and cystathionine γ-lyase (CSE) activity in pulmonary artery tissues were determined by biochemical method. CSE mRNA expression was detected by competitive reverse transcriptase-polymerase chain reaction (RT-PCR). Compared with control, LPS significantly increased mPAP [(1.82±0.29) kPa vs (1.43±0.26) kPa, P<0.01], decreased H2S production [(26.33±7.84) vs (42.92±8.73) pmol/g wet tissue per minute, P<0.01), and reduced endothelium-dependent relaxation response [(75.72±7.22)% vs (86.40±4.40) %, P<0.01) induced by ACh (1×10(-6) mol/L). These effects were partly reversed by co-administration of NaHS and enhanced by co-administration of PPG. Both CSE activity and CSE mRNA expression were consistent with H2S production. It is suggested that the inhibitory effect of LPS on endothelium-dependent relaxation results in pulmonary hypertension, which might be mediated through H(2)S.
