Division of Cardiology, Hospital for Sick Children, University of Toronto, Ontario, Canada.
J Thorac Cardiovasc Surg. 2012 Dec;144(6):1494-501. doi: 10.1016/j.jtcvs.2012.06.027. Epub 2012 Jul 18.
Chronic right ventricular (RV) pressure overload results in pathologic RV hypertrophy and diminished RV function. Although aortic constriction has been shown to improve systolic function in acute RV failure, its effect on RV responses to chronic pressure overload is unknown.
Adjustable vascular banding devices were placed on the main pulmonary artery and descending aorta. In 5 animals (sham group), neither band was inflated. In 9 animals (PAB group), only the pulmonary arterial band was inflated, with adjustments on a weekly basis to generate systemic or suprasystemic RV pressure at 28 days. In 9 animals, both pulmonary arterial and aortic devices were inflated (PAB + AO group), the pulmonary arterial band as for the PAB group and the aortic band adjusted to increase proximal systolic blood pressure by approximately 20 mm Hg. Effects on the functional performance were assessed 5 weeks after surgery by conductance catheters, followed by histologic and molecular assessment.
Contractile performance was significantly improved in the PAB + AO group versus the PAB group for both ventricles. Relative to sham-operated animals, both banding groups showed significant differences in myocardial histologic and molecular responses. Relative to the PAB group, the PAB + AO group showed significantly decreased RV cardiomyocyte diameter, decreased RV collagen content, and reduced RV expression of endothelin receptor type B, matrix metalloproteinase 9, and transforming growth factor β genes.
Aortic constriction in an experimental model of chronic RV pressure overload not only resulted in improved biventricular systolic function but also improved myocardial remodeling. These data suggest that chronically increased left ventricular afterload leads to a more physiologically hypertrophic response in the pressure-overloaded RV.
慢性右心室（RV）压力超负荷导致病理性 RV 肥厚和 RV 功能降低。虽然主动脉缩窄已被证明可改善急性 RV 衰竭时的收缩功能，但它对 RV 对慢性压力超负荷的反应的影响尚不清楚。
在主肺动脉和降主动脉上放置可调节的血管带装置。在 5 只动物（假手术组）中，两个带都没有充气。在 9 只动物（PAB 组）中，仅充气肺动脉带，每周调整以在 28 天时产生系统或超系统 RV 压力。在 9 只动物中，同时充气肺动脉和主动脉装置（PAB+AO 组），肺动脉带如 PAB 组，主动脉带调整以增加近端收缩压约 20mmHg。手术后 5 周通过传导导管评估功能性能，然后进行组织学和分子评估。
与 PAB 组相比，PAB+AO 组的收缩性能在两个心室均显著改善。与假手术动物相比，两个带组的心肌组织学和分子反应均有显著差异。与 PAB 组相比，PAB+AO 组 RV 心肌细胞直径明显减小，RV 胶原含量降低，内皮素受体 B、基质金属蛋白酶 9 和转化生长因子β基因的 RV 表达减少。
在慢性 RV 压力超负荷的实验模型中，主动脉缩窄不仅导致双心室收缩功能改善，而且改善心肌重构。这些数据表明，慢性左心室后负荷增加会导致压力超负荷 RV 出现更生理性的肥厚反应。
