Objective A rat model of cerebral small vessel disease (CSVD) was established by performing unilateral and single injection of sodium laurate through the internal carotid artery.The validity of the model was then assessed by analyzing of behavior scoring, cerebral infarction volume, cerebral microvascular density, hemodynamics, brain histopathology, and the expression of blood-brain barrier (BBB)-related protein.? Methods? Twelve SPF-grade male Sprague-Dawley (SD) rats were randomly divided into control group and model group, with six rats in each group. The model group received a single injection of 100 μL of sodium laurate (2 g/L) through 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 using enzyme-linked immunosorbent assay. Magnetic resonance imaging was used to detect cerebral infarction volume. Cerebral angiography was used to observe changes in cerebral vascular density. Ultrasonography was performed to measure the resistance index (RI) and perfusion index (PI). Histopathological changes in brain tissue were evaluated using hematoxylin and eosin (HE) staining. Immunohistochemical staining was used to detect the expression of cerebral microvascular marker CD31 and tight junction proteins ZO-1 and Occludin in the cortex of brain tissue.? Results? Compared to the control group, the Longa scores, postural reflex scores and cerebral infarction volumes were significantly increased (P<0.05), while the cerebral vascular density was decreased in the model group (P<0.05). The serum HCY levels, carotid RI, and PI values were all significantly increased in the model group (P<0.05). Additionally, HE staining revealed solidified neuronal nuclei and enlarged perivascular gaps in the cortex of brain tissues of the model group. The expression of CD31, ZO-1, and Occludin was significantly reduced in the cortex of brain tissues of the model group compared to the control group (P<0.05).? Conclusions? The rat model of CSVD can be rapidly and effectively established through unilateral and single injection of high-concentration sodium laurate via the internal carotid artery. This model, characterized by neurobehavioral abnormalities, cognitive impairment, cerebral infarction, insufficient cerebral blood supply, reduced vascular density, and disruption of the BBB, served as an effective rat model for the study of CSVD.