RIGHT VENTRICULAR DYSFUNCTION AFTER PRESSURE OVERLOAD

急性右室(RV)压力超负荷可能由以下原因引起 肺栓塞、缺氧性肺血管收缩、左心室 失败，或心脏移植后或延长 心肺转流术。房车压力过载可能导致房车故障 或功能障碍，是这些疾病发病和死亡的主要原因 条件。申请人的初步研究表明 右室收缩功能即使在恢复后仍保持低迷状态 正常加载条件。最近的证据表明，被动的 机械因素，如心肌蠕动，以及活动性 收缩过程，可能有助于下列收缩功能 急性右室压力过载。如果胶原蛋白结构被破坏 导致压力超负荷后右室功能障碍，然后是治疗 旨在保持细胞外基质的完整性可以 提供一种补充肌力刺激的治疗方式 在急性房车衰竭中。 将定量评估局部右室收缩功能 在开胸手术中使用压力段长度环分析 RV压力和体积过载的猪模型。组织学和 将进行胶原结构的超微结构测量 灌流固定后光镜和电子显微镜的观察 红心。然后组织学和超微结构测量将是 与心功能派生指数的变化有关， 确定胶原结构的特定变化是否会导致 心功能的可预测变化。

Acute right ventricular (RV) pressure overload may be caused by pulmonary embolism, hypoxic pulmonary vasoconstriction, left ventricular failure, or following cardiac transplantation or prolonged cardiopulmonary bypass. RV pressure overload may result in RV failure or dysfunction, and is a major cause of morbidity and mortality in these conditions. Preliminary studies by the applicant have demonstrated that RV systolic function remains depressed even after restoration of normal loading conditions. Recent evidence suggests that passive mechanical factors, such as myocardial creep, as well as active contractile processes, may contribute to systolic function following acute RV pressure overload. If disruption of collagen architecture contributes to RV dysfunction after pressure overload, then therapies directed at preserving the integrity of the extracellular matrix may provide a therapeutic modality complementary to inotropic stimulation in acute RV failure. Quantitative assessment of regional RV systolic function will be performed using pressure-segment length loop analysis in an open-chest pig model of RV pressure and volume overload. Histologic and ultrastructural measurements of collagen architecture will e performed using optical and electron microscopy following perfusion-fixation of hearts. The histologic and ultrastructural measurements will then be related to changes in derived indices of ventricular function, to determine whether specific changes in collagen architecture cause predictable changes in ventricular function.