Zhang Chao-Ying, Li Xiao-Hui, Zhang Ting, Fu Jin, Cui Xiao-Dai
Department of Cardiovascular Diseases, Children's Hospital Affiliated to the Capital Institute of Pediatrics, ChaoYang, Beijing 100020, P.R. China.
Central Laboratory of Infection and Immunity, Capital Institute of Pediatrics, ChaoYang, Beijing 100020, P.R. China.
Biomed Rep. 2013 May;1(3):454-458. doi: 10.3892/br.2013.87. Epub 2013 Mar 26.
The present study investigated the role of hydrogen sulfide (HS), a novel gaseous transmitter, in chronic heart failure (CHF) induced by left-to-right shunt, leading to volume overload. Thirty male Sprague-Dawley rats were randomly divided into four groups: the shunt group, the sham group, the shunt + sodium hydrosulfide (NaHS) group and the sham + NaHS group. CHF was induced in the rats by abdominal aorta-inferior vena cava shunt operation. Rats in the shunt + NaHS and sham + NaHS groups were injected intraperitoneally with NaHS (HS donor). Haemodynamic parameters were measured 8 weeks after surgery. In addition, left ventricular heme oxygenase (HO)-1 mRNA expression was measured by real-time PCR. Protein expression of HO-1 was evaluated by western blot analysis. Eight weeks after surgery, compared to the sham group, the left ventricular systolic pressure (LVSP) and left ventricular peak rate of contraction and relaxation (LV±dp/dtmax) were significantly reduced; the left ventricular end-diastolic pressure (LVEDP) was significantly increased in the shunt group (all P<0.05). However, NaHS increased LVSP and LV±dp/dtmax (all P<0.05) and decreased LVEDP (P<0.05). Protein expression of HO-1 was significantly decreased in the shunt group compared to that in the sham group (P<0.05). NaHS increased protein expression of HO-1 compared to that in the shunt group (P<0.05). HO-1 mRNA expression was significantly increased in the shunt + NaHS group compared to that in the shunt group (P<0.01). The present study demonstrated that HS may play a protective role in volume overload-induced CHF by upregulating protein and mRNA expression of HO-1.
本研究探讨了新型气体递质硫化氢（HS）在左向右分流所致慢性心力衰竭（CHF）（导致容量超负荷）中的作用。30只雄性Sprague-Dawley大鼠随机分为四组：分流组、假手术组、分流+硫氢化钠（NaHS）组和假手术+NaHS组。通过腹主动脉-下腔静脉分流手术诱导大鼠发生CHF。分流+NaHS组和假手术+NaHS组大鼠腹腔注射NaHS（HS供体）。术后8周测量血流动力学参数。此外，通过实时PCR检测左心室血红素加氧酶（HO）-1 mRNA表达。通过蛋白质印迹分析评估HO-1的蛋白表达。术后8周，与假手术组相比，分流组左心室收缩压（LVSP）、左心室收缩和舒张峰值速率（LV±dp/dtmax）显著降低；左心室舒张末期压力（LVEDP）显著升高（均P<0.05）。然而，NaHS可升高LVSP和LV±dp/dtmax（均P<0.05）并降低LVEDP（P<0.05）。与假手术组相比，分流组HO-1蛋白表达显著降低（P<0.05）。与分流组相比，NaHS可增加HO-1蛋白表达（P<0.05）。与分流组相比，分流+NaHS组HO-1 mRNA表达显著增加（P<0.01）。本研究表明，HS可能通过上调HO-1的蛋白和mRNA表达，在容量超负荷诱导的CHF中发挥保护作用。
