Brower G L, Henegar J R, Janicki J S
Department of Physiology and Pharmacology, Auburn University, Alabama 36849-5517, USA.
Am J Physiol. 1996 Nov;271(5 Pt 2):H2071-8. doi: 10.1152/ajpheart.1996.271.5.H2071.
The left ventricle (LV) significantly dilates and hypertrophies in response to chronic volume overload. However, the temporal responses in LV mass, volume, and systolic/diastolic function secondary to chronic volume overload induced by an infrarenal arteriovenous (A-V) fistula in rats have not been well characterized. To this end, LV end-diastolic pressure, size, and function (i.e., isovolumetric pressure-volume relationships in the blood-perfused isolated heart) were assessed at 1, 2, 3, 5, and 8 wk post-A-V fistula and compared with age-matched control animals. Progressive hypertrophy (192% at 8 wk), ventricular dilatation (172% at 8 wk), and a decrease in ventricular stiffness (257% at 8 wk) occurred in the fistula groups. LV end-diastolic pressure increased from a control value of 4.2 +/- 3.1 mmHg to a peak value of 15.7 +/- 3.6 mmHg after 3 wk of volume overload. A subsequent decline in LVEDP to 11.0 +/- 6.0 mmHg together with further LV dilation (169%) corresponded to a significant decrease in LV stiffness (222%) at 5 wk post-A-V fistula. Myocardial contractility, as assessed by the isovolumetric pressure-volume relationship, was significantly reduced in all A-V fistula groups; however, the compensatory remodeling induced by 8 wk of chronic biventricular volume overload tended to preserve systolic function.
左心室(LV)会因慢性容量超负荷而显著扩张和肥厚。然而,大鼠肾下动静脉(A-V)瘘引起的慢性容量超负荷继发的左心室质量、容积和收缩/舒张功能的时间反应尚未得到充分表征。为此,在A-V瘘形成后1、2、3、5和8周评估左心室舒张末期压力、大小和功能(即血液灌注离体心脏中的等容压力-容积关系),并与年龄匹配的对照动物进行比较。瘘管组出现渐进性肥厚(8周时为192%)、心室扩张(8周时为172%)和心室僵硬度降低(8周时为257%)。容量超负荷3周后,左心室舒张末期压力从对照值4.2±3.1 mmHg升至峰值15.7±3.6 mmHg。随后左心室舒张末期压力降至11.0±6.0 mmHg,同时左心室进一步扩张(169%),这与A-V瘘形成后5周左心室僵硬度显著降低(222%)相对应。通过等容压力-容积关系评估的心肌收缩力在所有A-V瘘管组中均显著降低;然而,8周慢性双心室容量超负荷引起的代偿性重塑倾向于保留收缩功能。