AI 中文总结
该研究构建首个完整肺循环搏动血流动力学数学模型，结合结构化树与毛细血管片模型，对比健康者与肺动脉高压患者模拟结果，显示纳入毛细血管改变血流动力学预测，还通过参数分析展示量化疾病能力。
AI 中文摘要
本研究提出了首个涵盖完整肺循环的搏动血流动力学数学模型，明确连接大动脉、小动脉、毛细血管、小静脉和大静脉。为克服先前模型排除明确毛细血管动力学的局限，采用一维结构化树模型与动态毛细血管片模型相结合的方法，建立将毛细血管片与结构化树耦合的递归方法。通过比较健康对照者和肺动脉高压患者模拟血流动力学评估该结构影响。结果表明，模型纳入毛细血管显著改变血流动力学预测。在健康对照者中，纳入毛细血管网络减弱搏动能量；在肺动脉高压患者中，明确建模毛细血管床纠正主肺动脉收缩压峰值预测过高问题，且肺动脉高压微血管重塑未能完全隔离静脉系统与动脉搏动。最后通过参数敏感性分析研究特定生物力学因素如何驱动血管重塑，证明该框架量化疾病进展和严重程度的能力。
英文摘要
This study presents the first mathematical model of pulsatile hemodynamics that encompasses the complete pulmonary circulation, explicitly linking the large arteries, arterioles, capillaries, venules, and large veins. To overcome the limitations of previous models that exclude explicit capillary dynamics, we incorporate a one-dimensional structured-tree model of the pulmonary arteries and veins with a dynamic capillary sheet model. This approach establishes a recursive method for coupling the capillary sheets to the structured trees, connecting arterioles and venules in a ladder-like architecture. To evaluate the impact of incorporating this capillary structure, we compare simulated hemodynamics in a healthy control subject and a pulmonary hypertension (PH) patient. Results illustrate that including capillaries in the model significantly alters hemodynamic predictions by introducing downstream damping. In the healthy control subject, the inclusion of the capillary network attenuates pulsatile energy, yielding the expected steady venous pressure and flow profiles, whereas omitting the capillaries results in an unphysiological high pulsatility transmitting into the venous system. The structural impact of the capillaries is even more pronounced in the PH patient, where explicitly modeling the capillary bed corrects an over-prediction in peak systolic pressure in the main pulmonary artery. Furthermore, unlike the healthy control subject, the remodeled PH microvasculature fails to completely isolate the venous system from arterial pulsations. Finally, we employ parametric sensitivity analysis to investigate how specific biomechanical factors drive vascular remodeling, demonstrating the framework's capability to quantify disease progression and severity.
