SUMMARY Since the 1980 s nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S), the endogenous gas molecules produced from metabolic pathway, have been realized as signal molecules to be involved in the regulation of body homeostasis and to play important roles under physiological and pathophysiological conditions. The researches on these endogenous gas signal molecules opened a new avenue in life science. To explore the new member of gasotransmitter family, other endogenous gas molecules which have been regarded as metabolic waste up to date, and their biological regulatory effects have been paid close attention to in the current fields of life science and medicine. Sulfur dioxide (SO2) can be produced endogenously from normal metabolism of sulfur-containing amino acids. L-cysteine is oxidized via cysteine dioxygenase to L-cysteinesulfinate, and the latter can proceed through transamination by glutamate oxaloacetate transaminase (GOT) to β-sulfinylpyruvate which decomposes spontaneously to pyruvate and SO2. In mammals, activated neutrophils by oxidative stress can convert H2S to sulfite through a reduced form of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase-dependent process. The authors detected endogenous production of SO2 in all cardiovascular tissues, including in heart, aorta, pulmonary artery, mesenteric artery, renal artery, tail artery and the plasma SO2 content. As the key enzyme producing SO2, GOT mRNA in cardiovascular system was detected and found to be located enrichedly in endothelial cells and vascular smooth muscle cells near the endothelial layer.When the normal rats were treated with hydroxamate(HDX), a GOT inhibitor, at a dose of 3.7 mg/kg body weight, the blood pressure (BP) went high markedly, the ratio of wall thickness to lumen radius was increased by 18.34%, and smooth muscle cell proliferation was enhanced. The plasma SO2 level in the rats injected with 125 μmol/kg body weight SO2 donor was increased to 721.98±30.11 μmol/L at the end of 30 seconds, while th
目的 研究二氧化硫（ SO2）对低氧性肺动脉高压大鼠肺动脉内源性硫化氢（H2S）/胱硫醚-γ-裂解酶（ CSE）以及H2S/巯基丙酮酸转硫酶（MPST）体系的调节作用.方法 将雄性Wistar大鼠（32只）随机分为对照组、低氧组、低氧＋ SO2组和低氧＋天冬氨酸异羟肟酸（hydroxamate,HDX）组,每组8只.低氧处理采用常压低氧的方法,氧浓度为10％,每天低氧6h,持续21 d.对照组大鼠在常氧环境中饲养.低氧处理结束后采用右心导管法测定肺动脉平均压,采用硫电极法测定肺组织H2S含量和H2S产率,采用免疫组化法检测各组大鼠肺小动脉内膜及中膜CSE和MPST的蛋白表达.结果 低氧组大鼠肺动脉平均压较对照组高[（33.38 ±6.32） mm Hg vs（16.74±3.81） mm Hg,1 mm Hg=0.133 kPa,P＜0.01]；低氧＋SO2组大鼠肺动脉平均压较低氧组低[（29.65±2.53）mm Hg vs（33.38±6.32） mm Hg,P＜0.01],低氧＋HDX组大鼠肺动脉平均压较低氧组高[（39.44±6.26） mm Hg vs（33.38±6.32） mm Hg,P＜0.01].低氧组大鼠肺组织H2S含量[（2.02±0.43） μmol/g vs （3.11±0.42） μmol/g,P＜0.01]及H2S产率[（19.64±3.48） nmol/（g· min）vs（28.20±5.95） nmol/（g·min）,P＜0.05]均较对照组低.给予SO2供体后,低氧＋SO2组肺组织H2S含量[（2.73±0.20）μmol/g vs（2.02±0.43）μmol/g,P＜0.01]及H2S产率[（26.24±1.92） nmol/（g· min）vs（19.64±3.48） nmol/（g· min）,P＜0.01]均较低氧组升高.当给予内源性SO2生成酶抑制剂HDX后,低氧＋HDX组肺组织H2S含量[（1.64±0.23） μmol/g vs （2.02±0.43）μmol/g,P＜0.05]及肺组织H2S产率[（13.94±3.63） nmol/（g·min） vs （19.64±3.48） nmol/（g·min）,P＜0.05]均较低氧组低.低氧组大鼠肺小动脉内膜[（0.31±0.02）vs（0.36±0.01）,P＜0.01]及中膜[（0.27±0.01）vs （0.30±0.01）,P＜0.01]中CSE蛋白表达均较对照组低.低氧＋SO2组大鼠肺小动脉内膜CSE蛋白表达较低氧组高[（0.35±0.02） vs （0.31 ±
