Objective To determine the relationship between the rennin-angiotensin-aldosterone systems(RAAS)and left atrial structure remodeling in patients with rheumatic mitral stenosis.Methods The patients with rheumatic mitral stenosis were divided into two groups according to atrial fibrillation:sinus rhythm group(SR group,n=25)and atrial fibrillation group(AF group,n=30).17 normal subjects were selected as normal control group(NC).The plasma concentration of renin,angiotonin Ⅱ(Ang Ⅱ)and aldosterone(Ald)were measured by radioimmunoassay(RIA).Results The average value of the left atrial diameter in AF group was significantly greater than that of both SR group and NC group,increased by 16.9%[(57.71±8.07)mm vs.(48.48±5.05)mm,P＜0.01)]and 87.8%(57.71±8.07 mm vs.30.18±2.85 mm,P＜0.01)respectively.Compared with NC group,the left atrial diameter of SR group was also significantly greater,elevated by 60.6%[(48.48±5.05)mm vs.(30.18±2.85)mm,P＜0.01)].The level of plasma rennin activity(PRA),Ang Ⅱ and Aid in AF and SR patients was significantly higher than those of NC subjects(P＜0.01),and compared with SR patients,the level of those in AF patients was also significantly increased(P＜0.01,P＜0.05).Pearson correlation analysis revealed a positive correlation between the plasma level of PRA,Ang Ⅱ or Ald and the value of the left atrial diameter(r=0.277,0.485,0.431,P＜0.05,P＜0.01,P＜0.01).Multiple liner stepwise regression analysis showed that plasma Ang Ⅱ and Ald were the important risk factors that affected left atrial diameter in patients with rheumatic mitral stenosis(Bate=0.362,0.261,P＜0.01,P＜0.05).Conclusion Patients with rheumatic mitral stenosis are characterized by the activation of circulating RAAS,and the plasma Ang Ⅱ and Ald may contribute to left atrial structure remodeling.

In this study, it is to compare the effectiveness of prevention against and treatment of doxorubicin (DOX) induced cardiotoxicity by dexrazoxane and schisandrin B (Sch B) in rats. Sprague-Dawley (SD) rats were randomly divided into the following 6 groups: normal saline group, DOX group, DOX+DEX group, DOX+Sch B (80 mg x kg(-1)) group, DOX+Sch B (40 mg x kg(-1)) group and DOX+Sch B (20 mg x kg(-1)) group. The results showed that Sch B could combat the increase of myocardial enzymes in peripheral blood, decrease of the enzyme activity of myocardial tissue antioxidant enzymes and disorders of systolic and diastolic function of heart in rats intravenously injected with doxorubicin (15 mg x kg(-1)). Sch B was better than DEX in protecting rat against DOX-induced the symptoms. Sch B could protect rat against DOX-induced acute cardiomyopathy and has clinical potential applications.