Objectives: The chicken umbilical artery floats in a fluid environment in the allantoic cavity that is similar to the human cerebral vessels in the subarachnoid space. Therefore, to simulate the pathological changes of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in humans, this study established an umbilical arterial vasospasm model induced by internal bleeding in the allantoic cavity of chicken embryos. Methods: We established an umbilical arterial vasospasm model using a needle puncture method on a vein in the chorioallantoic membrane (CAM) to induce a hemorrhage in the allantoic cavity of 11-day-old chicken embryonated eggs. The treated chicken embryos were sacrificed on days 1, 3, 5, and 7 post-hemorrhage to collect the umbilical artery samples. The pathological sections were prepared for hematoxylin-eosin (HE) staining, terminal deoxyribonucleotidyl transferase (TDT)-mediated dUTP nick end labeling (TUNEL) staining, and transmission electron microscope (TEM) observation to investigate the changes in the inner cross-sectional area (CSA), wall thickness, number of TUNEL-positive apoptotic cells in the vascular wall, and wall ultrastructure of the umbilical artery. Results: Compared with the control group, the experimental group showed no statistically significant difference in the inner CSA and wall thickness of the umbilical artery on day 1 post-hemorrhage. On days 3, 5, and 7 post-hemorrhage, the inner CSA of the umbilical artery was significantly smaller (P<0.05), and the umbilical artery had a thicker wall in the experimental group (P<0.05) versus the control group. TUNEL staining of the umbilical arterial sections revealed that, on days 3 and 5 post-hemorrhage, the apoptotic index of the umbilical arterial wall cells in the experimental group was remarkably higher than that in the control group (P<0.05). TEM observation of the umbilical arterial wall on day 5 post-hemorrhage revealed that, in the experimental group, the endothelial cells showed shrinkage and were loosely arranged, the normal intercellular connections were absent, the fragmented nuclear chromatin aggregated toward the nuclear membrane, and the subendothelial elastic layer exhibited wrinkles arranged in a wavy pattern. In the control group, the endothelial cells had oval nuclei and were arranged in a single layer with tight intercellular connections, and the subendothelial layer was evenly arranged and clearly structured. Conclusions: Our chicken embryo umbilical arterial vasospasm model, established by the needle puncture of CAM vessels to induce internal bleeding in the allantoic cavity, exhibits certain pathological changes similar to mammalian SAH-induced CVS, which makes it to be a promising in vivo model system for study of vasospasm.