Early right ventriculo-arterial uncoupling in borderline pulmonary hypertension on experimental heart failure
Early right ventriculo-arterial uncoupling in borderline pulmonary hypertension on experimental heart failure
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DOI：
10.1152/japplphysiol.00467.2010
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发表时间：
2010-10-01
影响因子：
3.3
通讯作者：
Naeije, Robert
中科院分区：
文献类型：
--
作者：
Pagnamenta, Alberto;Dewachter, Celine;Naeije, Robert
心力衰竭（HF）时的肺动脉高压限制了运动能力和生存率，可能是因为相关的右心室（RV）衰竭。本研究探讨了实验性心衰时右室功能对早期肺动脉高压的适应机制。在6只犬中进行7周的快速心室起搏，诱导了以心脏肥大和左心室射血分数降低为特征的HF。与8只对照犬相比，肺动脉高压处于临界状态，平均肺动脉压仅升高至23 +/-2（平均值+/-SE）mmHg。然而，肺血管阻抗谱整体上向更高的压力偏移，对照组0 Hz阻抗（电阻）增加至662 +/-69 vs. 455 +/-41 www.example.com（-5）. m（2）（P <0.01），对照组特征阻抗增加至183 +/-20 vs. 104 +/-7 dynes.cm（-5）. m（2）（P <0.01）。RV收缩末期弹性（Ees）无变化，但对照组动脉弹性（Ea）增加至1.8 ± 0.3 vs 0.9 ± 0.1 mmHg/ml，因此由Ees与Ea比值（Ees/Ea）定义的RV-动脉耦合降低至0.8 ± 0.1 vs 1.5 ± 0.1（P <0.01）。吸入一氧化氮，40 ppm或5 μ g/min硝普钠iv，不影响Ees/Ea。50毫克（iv）米力农通过Ees的单独增加将Ees/Ea增加至1.6 +/-0.2。我们的结论是，过度起搏引起的HF伴随着边缘性肺动脉高压，但深刻的RV-动脉解偶联RV收缩功能的失败，以适应肺动脉阻力和弹性增加的综合效应解释。
Pulmonary hypertension on heart failure (HF) limits exercise capacity and survival probably because of associated right ventricular (RV) failure. This study investigated the mechanisms of RV function adaptation to early pulmonary hypertension in experimental HF. Seven weeks of rapid ventricular pacing in six dogs induced a HF characterized by cardiomegaly and decreased left ventricular ejection fraction. Compared with eight control dogs, pulmonary hypertension was borderline, with a mean pulmonary artery pressure increased to only 23 +/- 2 (means +/- SE) mmHg. However, the pulmonary vascular impedance spectrum was globally shifted to higher pressures, with an increase in 0 Hz impedance (resistance) to 662 +/- 69 vs. 455 +/- 41 dynes.cm(-5).m(2) in controls (P < 0.01) and in characteristic impedance to 183 +/- 20 vs. 104 +/- 7 dynes.cm(-5).m(2) in controls (P < 0.01). There was no change in RV end-systolic elastance (Ees), but arterial elastance (Ea) was increased to 1.8 +/- 0.3 vs. 0.9 +/- 0.1 mmHg/ml in controls so that RV-arterial coupling defined by the Ees-to-Ea ratio (Ees/Ea) was decreased to 0.8 +/- 0.1 vs. 1.5 +/- 0.1 in controls (P < 0.01). Inhaled nitric oxide, 40 ppm or 5 mu g.kg(-1).min(-1) nitroprusside iv, did not affect Ees/Ea. Fifty milligrams (iv) of milrinone increased Ees/Ea to 1.6 +/- 0.2 by an isolated increase in Ees. We conclude that overpacing-induced HF is accompanied by a borderline pulmonary hypertension but profound RV-arterial uncoupling explained by the failure of RV systolic function to adapt combined effects of increased pulmonary arterial resistance and elastance.