title: [The relationship between endogenous hydrogen sulfide system and pulmonary hypertension induced by hypoxic hypercapnia].
abstract: OBJECTIVE
  To investigate the changes of the endogenous hydrogen sulfide(H2S) system in pulmonary hypertension induced by hypoxic hypercapnia (HHPH) in rats and approach the possible mechanisms.
  
  
  METHODS
  20 SD rats were randomly divided into control group (C) and hypoxic hypercapnia group (HH) (n=10). The changes of hemodynamics and the right ventricle/left ventricle + septum (RV/LV + SP) were measured. The ratio of vessel wall area and total area (WA/TA) of arteriae pulmonalis were observed under lightmicroscope. By using TdT-mediated dUTP nick end labeling (TUNEL) and immunocytochemistry techniques, apoptosis index (AI) and expression of Bcl-2, Bax protein in arteriae pulmonalis were tested. Plasma level of H2S and activity of H2S generating enzymes in homogenates of rat lung tissue were evaluated by sensitive modified sulfide electrode method. Cystathionine-gamma-lyase (CSE) mRNA in lung tissues was determined by RT-PCR.
  
  
  RESULTS
  The level of mean pulmonary arterial pressure(mPAP), WA/TA and RV/LV + SP were significantly higher in HH group than those in C group (P < 0.05 or P < 0.01). Compared with those in C group, the AI of arteriae pulmonalis in HH group were significantly lower; the expression of Bcl-2 protein increased while that of Bax protein decreased, and the ratio of Bax/Bcl-2 went up obviously (all P < 0.01). Plasma level of H2S, the activity of H2S generating enzymes and CSE mRNA in HH group were significantly lower than those in C group (all P < 0.01). Plasma level of H2S, the activity of H2S generating enzymes, CSE mRNA each was closely positively related to Al while inversely related to mPAP and Bcl-2/Bax (all P < 0.01).
  
  
  CONCLUSIONS
  The endogenous hydrogen sulfide system is closely related to pulmonary hypertension induced by hypoxic hypercapnia. The depression of the H2S/CSE system in HHPH may help increase the ratio of Bcl-2/Bax, inhibit apoptosis of pulmonary artery smooth muscle cells and finally result in the formation of pulmonary hypertension.
authors.affiliation: Department of Pathophysiology, Wenzhou Medical College, Wenzhou 325035, China. xu2000fly@126.com
authors.forename: Yi-xiao
authors.initials: YX
authors.lastname: Xu
authors.forename: Yuan-yuan
authors.initials: YY
authors.lastname: Wang
authors.forename: Xu-guang
authors.initials: XG
authors.lastname: Jia
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Lu
authors.initials: L
authors.lastname: Shi
authors.forename: Wan-tie
authors.initials: WT
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D006862:Hydrogen Sulfide / Q000378:metabolism*; D006935:Hypercapnia / Q000150:complications / Q000503:physiopathology*; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology*; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D006862:Hydrogen Sulfide