Grignola Juan C, Ginés Fernando, Bia Daniel, Armentano Ricardo
Departamento de Fisiología, Facultad de Medicina, Universidad de la República, Gral. Flores 2125 (11800), Montevideo, Uruguay.
Int J Cardiol. 2007 Feb 7;115(2):171-82. doi: 10.1016/j.ijcard.2006.03.007. Epub 2006 Jun 22.
Right ventricular adaptation to pulmonary hypertension (PH) is an important prognostic factor. Pulmonary artery (PA) smooth muscle activation attenuates arterial dysfunction during acute PH. We investigated the role of the pulmonary artery vascular smooth muscle activation on the right ventricular-vascular coupling during acute PH. PA flow, pressure, and diameter, right ventricular and aortic pressures were recorded in six anesthetized sheep. Acute PH was induced by phenylephrine (APH) and PA mechanical constriction (PPH). We calculated the PA buffering function, the incremental elastic modulus and pulmonary vascular compliance. Pulmonary vascular impedance and right ventricular hydraulic power were calculated through Fourier approach. We also quantified the magnitude and timing of the reflected wave. Right ventricular-vascular coupling was assessed by the energy transmission ratio. Pulmonary buffering function and vascular compliance increased (P<0.05) and arterial wall stiffness decreased (P<0.05) during APH with respect to PPH. Although total input resistance increased and reflected wave came back earlier during PH states (P<0.05), only PPH produced a rightward shift of the pulmonary impedance and a more prominent reflected wave. Accordingly, APH determined a minor increase of total hydraulic power with a smaller pulsatile to total power ratio and energy transmission ratio (P<0.05). In conclusion, isobaric PA vasoconstriction prevents the pulsatile hydraulic load to increase by preserving the PA buffering function and the reflected wave magnitude. Thus, vascular smooth muscle activation of the main PA improves the energy transfer from the right ventricle to the hypertensive pulmonary circulation, and this may play relevant role in the right ventricular adaptation to acute PH.
右心室对肺动脉高压（PH）的适应是一个重要的预后因素。肺动脉（PA）平滑肌激活可减轻急性PH期间的动脉功能障碍。我们研究了肺动脉血管平滑肌激活在急性PH期间对右心室-血管耦合的作用。记录了六只麻醉绵羊的PA血流、压力和直径、右心室和主动脉压力。通过去氧肾上腺素（APH）和PA机械收缩（PPH）诱导急性PH。我们计算了PA缓冲功能、增量弹性模量和肺血管顺应性。通过傅里叶方法计算肺血管阻抗和右心室水力功率。我们还量化了反射波的幅度和时间。通过能量传输比评估右心室-血管耦合。与PPH相比，APH期间肺缓冲功能和血管顺应性增加（P<0.05），动脉壁硬度降低（P<0.05）。虽然在PH状态下总输入阻力增加且反射波更早返回（P<0.05），但只有PPH导致肺阻抗向右移位且反射波更明显。因此，APH导致总水力功率的轻微增加，搏动功率与总功率之比和能量传输比更小（P<0.05）。总之，等压PA血管收缩通过保留PA缓冲功能和反射波幅度来防止搏动性水力负荷增加。因此，主PA的血管平滑肌激活改善了从右心室到高血压肺循环的能量传递，这可能在右心室对急性PH的适应中起相关作用。
