Magid N M, Young M S, Wallerson D C, Goldweit R S, Carter J N, Devereux R B, Borer J S
Division of Cardiology, Cornell University Medical College, New York Hospital--Cornell Medical Center, New York 10021.
J Mol Cell Cardiol. 1988 Mar;20(3):239-46. doi: 10.1016/s0022-2828(88)80056-7.
Aortic regurgitation was induced by retrograde perforation of an aortic valve cusp under hemodynamic guidance in 12 New Zealand White rabbits. Regurgitant fraction was documented by electromagnetic flow probe and six sham-operated animals served as controls. Two-dimensional, M-mode and Doppler echocardiography was performed pre-operatively and serially post-operatively for 3 to 6 months. Animals with aortic regurgitation developed progressive left ventricular dilatation and eccentric hypertrophy. Left ventricular internal dimension at end-diastole and left ventricular mass were increased from baseline values by 41 and 94% (P less than 0.001), respectively; fractional shortening was stable while end-systolic stress increased 50% (P less than 0.01. Thus, acutely induced aortic regurgitation in rabbits results in a chronic model which may be appropriate for stimulation of the hypertrophic response to aortic regurgitation in humans.
在血流动力学引导下，通过逆行穿刺12只新西兰白兔的主动脉瓣叶诱导主动脉瓣反流。用电磁血流探头记录反流分数，6只假手术动物作为对照。术前及术后连续3至6个月进行二维、M型和多普勒超声心动图检查。患有主动脉瓣反流的动物出现进行性左心室扩张和离心性肥厚。舒张末期左心室内径和左心室质量分别比基线值增加了41%和94%（P<0.001）；缩短分数稳定，而收缩末期应力增加了50%（P<0.01）。因此，兔急性诱导的主动脉瓣反流导致了一种慢性模型，该模型可能适用于激发人类对主动脉瓣反流的肥厚反应。
