Objective A rat model of cerebral small vessel disease (CSVD) was established by unilateral injection of a single dose of sodium laurate into the internal carotid artery. The effectiveness of the model was assessed by behavior scoring and analysis of serum-related indicators, cerebral infarction volume, cerebral microvascular density, hemodynamics, brain histopathology and the expression of blood-brain barrier (BBB)-related proteins. Methods SPF-grade male SD rats were divided randomly into a control group and a model group ( n= 6 per group). The model group received a single injection of 100 μL of sodium laurate (2 g/L) via the internal carotid artery, while the control group underwent the same surgical procedure but received an equal volume of saline. Neurobehavioral assessments were conducted using the Longa score and postural reflex test. Serum homocysteine (HCY) levels were measured by enzyme-linked immunosorbent assay. Cerebral infarction volume was detected by magnetic resonance imaging and changes in cerebral vascular density were observed by cerebrovascular imaging. The resistance index (RI) and perfusion index (PI) were measured by ultrasonography. Histopathological changes in brain tissue were evaluated by hematoxylin and eosin (HE) staining. Expression of the cerebral microvascular marker CD31 and tight junction proteins ZO-1 and Occludin in brain cortex tissue were detected by immunohistochemical staining. Results The Longa score, postural reflex score (P<0.05), and cerebral infarction volume were significantly increased (P<0.05) while the cerebral vascular density was decreased in the model group compared with the control group. Serum HCY levels, carotid RI, and PI values were all significantly increased in the model group (P<0.05). HE staining revealed solidified neuronal nuclei and enlarged perivascular spaces in the brain cortex in the model group. Immunohistochemical staining revealed that CD31, ZO-1, and Occludin expression were significantly reduced in the brain cortex in the model group compared with the control group (P<0.05). Conclusions A rat model of CSVD can be established rapidly and effectively by a single unilateral injection of high concentration sodium laurate via the internal carotid artery. This model is characterized by neurobehavioral abnormalities, cerebral infarction, insufficient cerebral blood supply, reduced vascular density, and disruption of the BBB, suggesting that it may serve as an effective rat model for the study of CSVD.