The selective laser melted (SLM) 316L stainless steel (316L SS) has shown superior tensile ductility and doubled yield strength compared to its wrought counterpart. The significantly improved yield strength has been attributed to the unique cellular substructures featured by Cr/Mo-segregation and trapped dislocations. The excellent ductility of SLMed 316L SS has been mainly understood from the pronounced deformation twinning, which, however, is just one of the dominant plastic deformation mechanisms in 316L SS. Here instead, we report two other fundamental deformation micro-mechanisms, i.e., deformation faulting and dislocation cell refinement, in the SLM 316L SS. Our results showed that deformation faulting and dislocation cell refinement characterize the whole tensile deformation significantly except for deformation twinning. These newly found mechanisms synergistically dominated the deformation behavior at low strain levels while deformation faulting and twinning play a crucial role at medium and high strain levels. The pre-existing stacking faults (SFs) in cellular substructure is mainly responsible for the significant deformation faulting. At the early deformation stage, these pre-existing SFs provide faulting nuclei for deformation faulting, leading to wide SFs. These wide SFs in different cellular interiors penetrate the cellular boundaries and overlap as the strain increases, resulting in long stacking fault ribbons (SFRs). We attributed the formation of DCs to the measured medium stacking fault energy (SFE) of ∼18 mJ/m². Upon straining, equiaxed dislocation cells (DCs) were generated by new dislocation cell walls (DCWs) inside the cellular substructure, and refined by either the dissociation of fully developed DCWs or the continuously formed new DCWs. Together with deformation twinning, these two fundamental deformation mechanisms jointly led to a steady strain hardening rate during tension and thus a superior tensile ductility of the SLM 316L SS with high yield strength. These findings provide new insights into the excellent strength-ductility combination of SLMed 316L SS and the experimental basis for crystal plasticity modeling and simulation, as well.

与锻造不锈钢相比，选择性激光熔化 (SLM) 316L 不锈钢 (316L SS) 具有出色的拉伸延展性和两倍的屈服强度。屈服强度的显着提高归因于以 Cr/Mo 偏析和捕获位错为特征的独特蜂窝亚结构。SLMed 316L SS 优异的延展性主要是通过明显的变形孪晶来理解的，然而，这只是 316L SS 的主要塑性变形机制之一。相反，我们在 SLM 316L SS 中报告了另外两个基本变形微观机制，即变形断层和位错单元细化。我们的结果表明，除了变形孪晶外，变形断层和位错单元细化显着表征了整个拉伸变形。这些新发现的机制协同主导了低应变水平下的变形行为，而变形断层和孪晶在中高应变水平下起着至关重要的作用。蜂窝子结构中预先存在的堆垛层错（SFs）是造成显着变形断层的主要原因。在早期变形阶段，这些预先存在的SFs为变形断层提供了断核，导致了宽SFs。不同细胞内部的这些宽 SF 穿透细胞边界并随着应变的增加重叠，导致长的堆垛层错带 (SFR)。我们将 DCs 的形成归因于测量的 18 mJ/m2 的介质堆垛层错能 (SFE) 蜂窝子结构中预先存在的堆垛层错（SFs）是造成显着变形断层的主要原因。在早期变形阶段，这些预先存在的SFs为变形断层提供了断核，导致了宽SFs。不同细胞内部的这些宽 SF 穿透细胞边界并随着应变的增加重叠，导致长的堆垛层错带 (SFR)。我们将 DCs 的形成归因于测量的 18 mJ/m2 的介质堆垛层错能 (SFE) 蜂窝子结构中预先存在的堆垛层错（SFs）是造成显着变形断层的主要原因。在早期变形阶段，这些预先存在的SFs为变形断层提供了断核，导致了宽SFs。不同细胞内部的这些宽 SF 穿透细胞边界并随着应变的增加重叠，导致长的堆垛层错带 (SFR)。我们将 DCs 的形成归因于测量的 18 mJ/m2 的介质堆垛层错能 (SFE) 导致长堆垛层错带（SFR）。我们将 DCs 的形成归因于测量的 18 mJ/m2 的介质堆垛层错能 (SFE) 导致长堆垛层错带（SFR）。我们将 DCs 的形成归因于测量的 18 mJ/m2 的介质堆垛层错能 (SFE)² . 应变后，等轴位错细胞 (DCs) 由细胞亚结构内的新位错细胞壁 (DCWs) 生成，并通过完全发育的 DCWs 的解离或不断形成的新 DCWs 进行细化。与变形孪晶一起，这两种基本变形机制共同导致在拉伸过程中稳定的应变硬化率，因此 SLM 316L SS 具有优异的拉伸延展性和高屈服强度。这些发现为 SLMed 316L SS 的优异强度-延展性组合以及晶体塑性建模和模拟的实验基础提供了新的见解。