中文摘要：

目的 观察单纯腹主动脉缩窄造成的心肌肥厚能否转变成为心力衰竭.方法 实验选用8周龄的Wistar大鼠,使用7-0号尼龙线对其肾上腹主动脉进行缩窄手术,造成后负荷性心肌肥厚模型（LVH,n=10）,同时设置假手术组（Sham,n=10）和正常组（Con,n=10）作为对照.术后第20周和第38周使用超声多普勒和多导生理仪对大鼠血流动力学进行检测.解剖后取出心脏,计算心脏/体重比,并通过HE染色和天狼猩红染色观察心脏形态和纤维化程度.结果 腹主动脉结扎后第20周,LVH组大鼠心室壁肥厚,舒张功能下降（E/A ratio：LVH组：1.0 ±0.25,Con组：1.6±0.12）.术后38周,左心室壁肥厚程度有所下降,但是心室腔扩大,心脏收缩和舒张功能明显下降（EF：LVH组：44.8±8.42,Con组：70.9±5.19;Max dP/dt：LVH组：4916±1267.3,Con组：14225±932.1;Min dP/dt：LVH组：-3246±1217.3,Con组：-12138±725.2）.腹主动脉缩窄术后的动物心脏重量明显增加（3.58±0.32 vs.2.34±0.15）,HE染色和天狼猩红染色显示LVH组大鼠在术后38周心脏纤维化明显.结论 腹主动脉缩窄造成的后负荷增高动物模型首先出现向心性心肌肥厚,伴以舒张功能下降,进而收缩功能下降,发展为心力衰竭.

英文摘要：

Objective To investigate whether chronic pressure-overload induced by suprarenal abdominal aortic banding may progress into left ventrieular failure in animal model. Methods Eight-week old male Wistar rats were enrolled and suprarenal abdominal aorta was ligated by 7-0 nylon suture against a 23-gauge needle. Rats with LV hypertrophy （LVH, n = 10）, agematched sham-operated rats （Sham, n = 10） and normal control rats （Con, n = 10） were assessed at 20 and 38 weeks after aortic banding. The ratio of heart weight to body weight was calculated and cardiac hemodynamic parameters were obtained bsy multi-functional physiology recorder and eehoeardiography. H.E. and pierosirius red staining methods were used to display collagen content in the rat hearts. Results Twelve weeks after banding, LVH rats showed LV wall hypertrophy with normal cavity dimensions and decreased diastolic function （E/A ratio： LVH： 1.0 ± 0.25, Con： 1.6 ± 0.12） . After 38 weeks of pressure overload, LV wall thickness was decreased and cavity dilated with a fall in left ventrieular ejection fraction, and further deterioration of systolic and diastolic function was evident（EF： LVH：44.8 ± 8.42, Con： 70.9 ± 5.19; Max dP/dt： LVH：4916 ± 1267.3, Con： 14225 ± 932.1 ; Min dP/dt： LVH ：3246 ± 1217.3, Con：-12138 ± 725.2）. In contrast to LVH rats, the shamoperated rats showed no change in LV dlastolie cavity dimension, and systolic and diastolic functions did not deteriorate or improved. H.E. and pierosirius red staining showed severe fibrosis in heart tissue of LVH animals. Conclusions This model of pressure overload is characterized initially by concentric LV hypertrophy with compensated LV chamber performance; however, markedly abnormal diastolic filling is present. The transition from compensated hypertrophy to heart failure is gradually emerged with LV dilation and impairment of systolic function.