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右心室压力负荷增加时的左心室尺寸及功能

Left ventricular dimensions and function during right ventricular pressure overload.

作者信息

Badke F R

出版信息

Am J Physiol. 1982 Apr;242(4):H611-8. doi: 10.1152/ajpheart.1982.242.4.H611.

DOI:10.1152/ajpheart.1982.242.4.H611
PMID:7065274
Abstract

The effects of right ventricular (RV) pressure overload on left ventricular (LV) function is controversial. Therefore, we examined LV dimensions and shortening after acute and chronic pulmonary artery (PA) constriction in six conscious dogs, preinstrumented with LV and RV catheters, an LV micromanometer, a PA inflatable cuff occluder, and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, and a free wall segment chord. Studies were performed before, immediately after, and 2, 4, and 6 wk after PA constriction. With acute cuff inflation, RV systolic- and end-diastolic pressures rose, but LV end-diastolic pressure fell. Both septal-lateral end-diastolic length and systolic shortening declined 4.1 +/- 0.7 mm and 5.9 +/- 2.3% respectively (P less than 0.01), whereas the anteroposterior and segment chords were unaffected. With chronic RV pressure overload septal-lateral shortening but not end-diastolic length returned to control levels. Also the first derivative of LV pressure (LV dP/dt) fell 540 +/- 164 mmHg/s by 6 wk compared with control, but this decline was reversed by volume expansion with dextran. We conclude that RV pressure overload displaces the septum toward the LV free wall; acutely this displacement is primarily at end diastole, but chronically it occurs at end systole as well, maintaining the septal contribution to LV ejection. Thus chronic RV pressure overload is associated with significant changes in LV diastolic shape but maintenance of normal LV function.

摘要

右心室(RV)压力超负荷对左心室(LV)功能的影响存在争议。因此,我们在6只清醒犬身上进行了研究,这些犬预先植入了左心室和右心室导管、左心室微测压计、肺动脉可充气袖带阻塞器以及超声晶体,以测量左心室前后径、室间隔-侧壁径和游离壁节段弦长。在肺动脉缩窄前、缩窄后即刻、以及缩窄后2周、4周和6周进行了研究。急性袖带充气时,右心室收缩压和舒张末期压力升高,但左心室舒张末期压力下降。室间隔-侧壁舒张末期长度和收缩期缩短分别下降了4.1±0.7mm和5.9±2.3%(P<0.01),而前后径和节段弦长未受影响。慢性右心室压力超负荷时,室间隔-侧壁缩短恢复到对照水平,但舒张末期长度未恢复。此外,与对照相比,6周时左心室压力的一阶导数(LV dP/dt)下降了540±164mmHg/s,但右旋糖酐扩容可逆转这种下降。我们得出结论,右心室压力超负荷使室间隔向左心室游离壁移位;急性时这种移位主要发生在舒张末期,但慢性时在收缩末期也会发生,从而维持室间隔对左心室射血的贡献。因此,慢性右心室压力超负荷与左心室舒张期形态的显著变化相关,但左心室功能维持正常。

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