二氧化硫对自发性高血压大鼠血压及血管结构的影响

The effect of sulfur dioxide on blood pressure and aortic structure of spontaneously hypertensive rat

目的研究二氧化硫(SO2)对自发性高血压大鼠(spontaneously hypertensive rat,SHR)血压以及平滑肌细胞增殖的影响。方法4wk♂SHR16只,随机分为SHR对照组(n=8)、SHR+Na2SO3/NaHSO3组(n=8),同样周龄(n=8)正常血压的Wistar-Kyoto(WKY)大鼠8只为正常对照组。5wk后检测各组大鼠血压,应用图像采集与分析系统对Hart′s改良弹力纤维染色的胸主动脉显微形态结构做定量分析,应用免疫组织化学方法检测平滑肌细胞增殖指数。结果9wk时SHR对照组血压高于WKY对照组大鼠(P<0·01);SHR+Na2SO3/NaHSO3组大鼠的血压较SHR对照组降低(P<0·01)。SHR对照组左心室与全心重量比高于WKY对照组大鼠(P<0·05)。SHR对照组胸主动脉中膜厚度与内径之比高于WKY对照组大鼠(P<0·01)。SHR+Na2SO3/NaHSO3组大鼠胸主动脉的中膜压力、中膜厚度与内径之比低于SHR对照组大鼠(P<0·01)。SHR对照组主动脉平滑肌细胞PI高于WKY对照组大鼠(P<0·01),SHR+Na2SO3/NaHSO3组PI低于SHR对照组(P<0·01)。结论SO2通过扩张血管和抑制血管平滑肌细胞增殖,参与缓解自发性高血压的形成及主动脉结构重塑。

Aim To investigate the effect of sulfur dioxide （SO2 ） on blood pressure and aortic structure of the spontaneous hypertensive rat （ SHR ）. MethodsSixteen male SHRs at the age of 4 weeks were randomly divided into SHR control group and SHR ＋ Na2SO3/ NaHSO3 group, respectively. Another eight male WKY rats served as WKY control group. Five weeks later, the blood pressure was determined. The rat aortas were dyed with Hart＇s Method. The morphometric parameters including outer radius, lumen radius and the wall thickness were calculated by Leica workstation. The proliferative index （PI） of smooth muscle cells was detected by immunohistochemical assay. Results The blood pressure of SHR control increased compared with that of WKY control rats （ P 〈 0. 01 ）. The blood pressure of SHR ＋ Na2SO3/NaHSO3 groups decreased compared with those of SHR control group（P 〈0.01 ）. The ratio of media to lumen radius in SHR control group was higher than that of WKY control rats（P 〈0. 01 ）. The ratio of media to lumen radius and the pressure of the media in SHR ＋ Na2SO3/NaHSO3 group were lower than those of SHR control group. The PI in aorta of SHR ＋ Na2SO3/NaHSO3 group and WKY control rats was higher than that of SHR control（P 〈0. 01 ）. Conclusions Sulfur dioxide was involved in the regulation of vascular structural remodeling in aorta by inhibiting the vascular smooth muscle cell proliferation in SHR.