甲亢源性心房颤动与肾素-血管紧张素系统相关发病机制的研究.

To study the pathogenesis of high thyroxine induced atrial fibrillation and renin-angiotension system (RAS). The model of hyperthyroid atrial fibrillation was made by injecting levothyroxine into abdominal cavity of rabbits, at the same time, irbesartan was infused into the stomach through gastric tube, and drug intervention was carried out in the left atrial myocyte culture of suckling rabbits. The induction rate of atrial fibrillation and apoptosis of left atrial myocytes were measured, RAS related cytokines and apoptotic protein expression were measured. The induced rate of atrial fibrillation in the withdrawal group, irbesartan group and control group was lower than that in the continuous administration group (P<0.05). The cardiomyocyte apoptosis rate, relative expression of ACE mRNA, ACE plasma concentration, expression amount, AngⅡ plasma concentration and expression amount in the with drawal group, the continuous administration group and the irbesartan group were higher than those in the control group, and those in the continuous administration group were higher than those in the withdrawal group and the irbesartan group (P<0.05). The relative expression of PARP and caspase3 in the withdrawal group, the continuous administration group and the irbesartan group were higher than those in the control group, and those in the continuous administration group were higher than those in the withdrawal group and the irbesartan group (P<0.05). The apoptosis rate of left atrial myocytes in AngⅡ group was higher than that in control group and thyroxine group after drug intervention (P<0.05). One of the pathogenesis of high thyroxine induced atrial fibrillation may be that it indirectly overactivates RAS, increases the expression of AngⅡin circulation and tissue, the latter induces apoptosis of atrial myocytes and electrical anatomical remodeling of left atrium. [ABSTRACT FROM AUTHOR]