The tumor microenvironment is abnormal and associated with tumor tissue hypoxia, immunosuppression, and poor response to treatment. One important abnormality present in tumors is vessel compression. Vessel decompression has been shown to increase survival rates in animal models via enhanced and more homogeneous oxygenation. However, our knowledge of the biophysical mechanisms linking tumor decompression to improved tumor oxygenation is limited. In this study, we propose a computational model to investigate the impact of vessel compression on red blood cell (RBC) dynamics in tumor vascular networks. Our results demonstrate that vessel compression can alter RBC partitioning at bifurcations in a hematocrit-dependent and flow rate–independent manner. We identify RBC focusing due to cross-streamline migration as the mechanism responsible and characterize the spatiotemporal recovery dynamics controlling downstream partitioning. Based on this knowledge, we formulate a reduced-order model that will help future research to elucidate how these effects propagate at a whole vascular network level. These findings contribute to the mechanistic understanding of hemodilution in tumor vascular networks and oxygen homogenization following pharmacological solid tumor decompression.

肿瘤微环境异常，与肿瘤组织缺氧、免疫抑制、治疗反应差有关。肿瘤中存在的一种重要异常是血管受压。血管减压已被证明可以通过增强和更均匀的氧合作用提高动物模型的存活率。然而，我们对将肿瘤减压与改善肿瘤氧合联系起来的生物物理机制的了解是有限的。在这项研究中，我们提出了一个计算模型来研究血管压缩对肿瘤血管网络中红细胞 (RBC) 动力学的影响。我们的结果表明，血管压缩可以以依赖于血细胞比容和与流速无关的方式改变分叉处的 RBC 分配。我们将跨流线迁移引起的 RBC 聚焦确定为负责并表征控制下游分区的时空恢复动态的机制。基于这些知识，我们制定了一个降阶模型，这将有助于未来的研究阐明这些影响如何在整个血管网络级别传播。这些发现有助于对肿瘤血管网络中的血液稀释和药物实体瘤减压后的氧均质化的机制理解。