房颤进展过程中犬左、右房心肌结构重构及超微结构的变化的不均一性

The heterogeneity of left and right atrial myocardial structural remodeling and ultrastructural changes in canines during the progression of atrial fibrillation

目的探讨犬快速右心房起搏诱发房颤48 h及8周后,心房肌结构重构包括心肌组织形态、糖原聚集情况和超微结构的变化及左、右心房变化的不均一性。方法成年比格犬在全麻下用快速右心房起搏(600次/min)建立房颤模型,对比格犬进行分组,分为对照组(control组)、48 h房颤组(48 h AF组)、8周房颤组(8 w AF组),每组各6只,分别取左右心房肌组织,行HE染色、糖原染色、马松(Masson)染色及透射电镜检查。观察随着房颤持续时间的延长,左、右心房组织大体结构,糖原沉积纤维化程度及超微结构的变化。结果随着房颤时间的延长,心房肌逐渐出现心肌纤维排列紊乱,心肌细胞数目减少,结缔组织增生。control组左房糖原累积程度高于右房,差异具有统计学意义(P<0.05),在48 h AF组及8 w AF组糖原沉积及纤维化较control组明显增加,8 w AF组较48 h AF组更为明显,差异具有统计学意义(P<0.05)。随着房颤时间的延长,心房肌逐渐出现线粒体肿胀变长,体积增大,基质变淡,线粒体脊密度减低,肌丝排列紊乱。闰盘扭曲模糊、不连续。结论随着房颤持续时间的延长,心房肌组织逐渐出现结构重构,心肌细胞排列紊乱,糖原聚集,线粒体异常及闰盘排列紊乱,为房颤的维持提供了基质。

Objective To explore the heterogeneity of left and right atrial myocardial structural remodeling and ultrastructural changes including morphological, glycogen and collagen deposition and ultrastructural changes in canines during the progression of atrial fibrillation(AF). Methods Under pentobarbital anesthesia, AF model was established by rapid right atrial pacing(600 beats/min). Eighteen Beagle dogs were randomly divided into three groups: control group,48 h AF group,8 w AF group,6 in each group. Tissues were obtained from the left and right atrium(LA/RA). HE stain, Periodic acid Schiff(PAS) and Masson’s trichrome staining of the LA/RA from each group were undertaken. The changes of the general structure and glycogen of the atrial tissue, the degree of fibrosis and the changes in ultrastructure with the progress of AF were observed. Results With the development of AF, the myocardial fiber arrangement disordered and the number of myocardial cells decreases. In control group, the degree of left atrial glycogen accumulation was higher than that of right atrial(P<0.05). Glycogen deposition and fibrosis were significantly increased at 48 h and 8 w after pacing, and that were more obvious in 8 w group than in 48 h group(P<0.05). Atrial cardiomyocytes gradually showed mitochondrial swelling and lengthening, increased volume, decreased matrix and density of mitochondrial ridge, and disordered arrangement of myofilaments. The leap disc is distorted, fuzzy and discontinuous. Conclusion With the prolongation of the AF duration, atrial tissue structural remodeling occurs gradually. The evidence demonstrates that disorder of myocardial cells, glycogen accumulation and fibrosis, mitochondrial abnormalities and disordered arrangement of discs as factors in the persistent of AF.