Kihara Y, Sasayama S, Miyazaki S, Onodera T, Susawa T, Nakamura Y, Fujiwara H, Kawai C
Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
Circ Res. 1988 Mar;62(3):543-53. doi: 10.1161/01.res.62.3.543.
The manner in which the left atrium adapts to chronic mitral regurgitation and the role of the adapted left atrium as a modulator of excessive central blood volume were analyzed in seven conscious dogs, instrumented with high-fidelity pressure transducers and ultrasonic dimension gauges for measurement of left atrial and left ventricular pressure and cavity size. After obtaining data in a control situation, mitral regurgitation was produced by transventricular chordal sectioning. Heart rate was matched by right atrial pacing. In the "early" stage (7-14 days), left ventricular end-diastolic and mean left atrial pressures increased from 6 to 16 mm Hg and from 4 to 12 mm Hg, respectively. Both left ventricular end-diastolic segment length and left atrial diameter prior to atrial contraction increased by 7%. In the "late" stage (20-35 days), despite significant decreases in left ventricular filling pressure (11 mm Hg) and left atrial pressure (8 mm Hg), there was a continuous increase in left ventricular end-diastolic dimension (10%) and atrial end-diastolic diameter (10%). After the onset of mitral regurgitation, the left atrium performed greater work with a more enlarged cavity. Left atrial chamber stiffness was progressively decreased. These changes were associated with progressive increase in the left atrial diameter at zero stress, and there was a significant increase in the diameter of the left atrial myocyte. These results indicate that during chronic mitral regurgitation, the left atrium enlarges in size and mass, with a more potent booster action. The left atrial chamber becomes more compliant. Thus, the enlarged left atrium appears to exert an important compensatory mechanism in the case of excessive central blood volume by buffering pressure rise in the atrium and by providing an adequate ventricular filling volume.
在七只清醒犬中分析了左心房适应慢性二尖瓣反流的方式以及适应后的左心房作为过多中心血容量调节因子的作用。这些犬植入了高保真压力传感器和超声尺寸测量仪，用于测量左心房和左心室压力及腔室大小。在获得对照情况下的数据后，通过经心室切断腱索产生二尖瓣反流。通过右心房起搏使心率匹配。在“早期”阶段（7 - 14天），左心室舒张末期压力和平均左心房压力分别从6 mmHg升高至16 mmHg和从4 mmHg升高至12 mmHg。心房收缩前的左心室舒张末期节段长度和左心房直径均增加了7%。在“晚期”阶段（20 - 35天），尽管左心室充盈压（11 mmHg）和左心房压力（8 mmHg）显著降低，但左心室舒张末期内径（10%）和心房舒张末期直径（10%）持续增加。二尖瓣反流发生后，左心房在腔室更大的情况下做功增加。左心房腔室僵硬度逐渐降低。这些变化与零应力下左心房直径的逐渐增加相关，并且左心房肌细胞直径显著增加。这些结果表明，在慢性二尖瓣反流期间，左心房在大小和质量上增大，具有更强的助推作用。左心房腔室变得更顺应。因此，在中心血容量过多的情况下，增大的左心房似乎通过缓冲心房压力升高和提供足够的心室充盈量发挥重要的代偿机制。
