Hennein H A, Jones M, Stone C D, Clark R E
Surgery Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20894.
J Thorac Cardiovasc Surg. 1993 Apr;105(4):624-32.
Left ventricular function in mitral regurgitation has typically been studied in models that either sever the chordae tendineae or create a ventriculoatrial shunt. These methods may have adverse effects on left ventricular function independent of the regurgitant lesion. An animal model of chronic mitral regurgitation was therefore developed that both preserves annuloventricular continuity and avoids the use of external shunts. A circular 0.16 to 0.24 mm/kg defect was created in the anterior mitral valve leaflet of weanling sheep under direct vision with the aid of cardiopulmonary bypass. Six animals were studied preoperatively and immediately postoperatively (acute regurgitation group), and 20 animals were studied 8.1 +/- 0.2 (mean +/- one standard deviation) months postoperatively (chronic regurgitation group). Animals with chronic mitral regurgitation were compared with an age- and weight-matched control group that was not operated on (n = 7). Volumetric data and ejection fraction were derived from digitalized cineangiographic images. Maximal elastance was calculated from pressure-volume loops obtained from the simultaneous recording of left ventricular pressure by micromanometer-tipped left ventricular catheters, and volumes were obtained from digitalized images of epicardial echocardiographic recordings. Mitral valve perforation resulted in 3+ to 4+ mitral regurgitation and a calculated regurgitant fraction of 37% +/- 7% (mean +/- one standard deviation). Acute mitral regurgitation was associated with an increase in left ventricular end-diastolic volume from 110 +/- 17 to 121 +/- 23 ml (p < or = 0.05) and no change in end-systolic volume. These changes were associated with an increase in fractional shortening, from 29% +/- 11% to 40% +/- 10% (p < or = 0.05), and an increase in velocity of circumferential shortening, from 1.5 +/- 0.7 to 2.9 +/- 0.7 circ/sec (p < or = 0.05). However, there was no change in maximal elastance, a load-independent index of left ventricular function. Conversely, animals with chronic mitral regurgitation exhibited an elevated end-diastolic volume (202 +/- 32 versus 145 +/- 34, p < or = 0.05), an elevated end-systolic volume (104 +/- 17 versus 63 +/- 20 ml, p < or = 0.05), and a reduced ejection fraction (48% +/- 6% versus 57% +/- 9%, p < or = 0.05) compared with controls.(ABSTRACT TRUNCATED AT 400 WORDS)
二尖瓣反流时左心室功能的研究通常采用切断腱索或建立心室-心房分流的模型。这些方法可能会对左心室功能产生独立于反流病变的不良影响。因此，开发了一种慢性二尖瓣反流动物模型，该模型既能保持房室连续性，又避免使用外部分流。在体外循环辅助下直视操作，在断奶绵羊的二尖瓣前叶制造一个直径0.16至0.24mm/kg的圆形缺损。对6只动物进行术前和术后即刻研究（急性反流组），20只动物在术后8.1±0.2（均值±一个标准差）个月进行研究（慢性反流组）。将慢性二尖瓣反流动物与未手术的年龄和体重匹配的对照组（n = 7）进行比较。容积数据和射血分数来自数字化电影血管造影图像。最大弹性由通过微测压尖端左心室导管同步记录左心室压力获得的压力-容积环计算得出，容积由心外膜超声心动图记录的数字化图像获得。二尖瓣穿孔导致3+至4+级二尖瓣反流，计算得出的反流分数为37%±7%（均值±一个标准差）。急性二尖瓣反流与左心室舒张末期容积从110±17ml增加到121±23ml（p≤0.05）相关，而收缩末期容积无变化。这些变化与缩短分数增加相关，从29%±11%增加到40%±10%（p≤0.05），圆周缩短速度增加，从1.5±0.7增加到2.9±0.7周/秒（p≤0.05）。然而，左心室功能的负荷独立指标最大弹性没有变化。相反，与对照组相比，慢性二尖瓣反流动物表现出舒张末期容积升高（202±32对145±34，p≤0.05）、收缩末期容积升高（104±17对63±20ml，p≤0.05）和射血分数降低（48%±6%对57%±9%，p≤0.05）。（摘要截取自400字）
