ATP release by red blood cells (RBCs) under shear stress (SS) plays a pivotal role in endothelial biochemical signaling cascades. The aim of this study is to investigate through numerical simulation how RBC spatiotemporal organization depends on flow and geometrical conditions to generate ATP patterns. Numerical simulations were conducted in a straight channel by considering both plasma and explicit presence of RBCs, their shape deformation and cell-cell interaction, and ATP release by RBCs. Two ATP release pathways through cell membrane are taken into account: pannexin 1 channel, sensitive to SS, and cystic fibrosis transmembrane conductance regulator, which responds to cell deformation. Several flow and hematocrit conditions are explored. The problem is solved by the lattice Boltzmann method. Application of SS to the RBC suspension triggers a nontrivial spatial RBC organization and ATP patterns. ATP localizes preferentially in the vicinity of the cell-free layer close to channel wall. Conditions for maximal ATP release per cell are identified, which depend on vessel size and hematocrit Ht. Increasing further Ht beyond optimum enhances the total ATP release but should degrade oxygen transport capacity, a compromise between an efficient ATP release and minimal blood dissipation. Moreover, ATP is boosted in capillaries, suggesting a vasomotor activity coordination throughout the resistance network.

剪切应力 (SS) 下红细胞 (RBC) 释放的 ATP 在内皮生化信号级联中起关键作用。本研究的目的是通过数值模拟研究 RBC 时空组织如何依赖流动和几何条件来生成 ATP 模式。通过考虑血浆和红细胞的显式存在、它们的形状变形和细胞-细胞相互作用以及红细胞的 ATP 释放，在直通道中进行数值模拟。考虑到通过细胞膜的两种 ATP 释放途径：pannexin 1 通道，对 SS 敏感，以及对细胞变形作出反应的囊性纤维化跨膜电导调节剂。探索了几种流量和血细胞比容条件。该问题由格子玻尔兹曼方法解决。将 SS 应用于 RBC 悬浮液会触发非平凡的空间 RBC 组织和 ATP 模式。ATP 优先定位在靠近通道壁的无细胞层附近。确定每个细胞最大 ATP 释放的条件，这取决于血管大小和血细胞比容高温。进一步增加Ht超过最佳值会增强总 ATP 释放，但会降低氧气运输能力，这是有效 ATP 释放和最小血液耗散之间的折衷。此外，毛细血管中的 ATP 增加，表明整个阻力网络中的血管舒缩活动协调。