This study was conducted to investigate whether the intraparenchymal and extraparenchymal portions of small cerebral arteries show different histopathological changes after subarachnoid hemorrhage (SAH). SAH was produced in dogs by a two-hemorrhage method, and the dogs were perfusion-fixed at 7 and 14 days after SAH. Normal untreated animals were also examined to determine whether or not the histological and morphological changes in the perforating arteries were affected by the perfusion pressure during perfusion-fixation. Control dogs, which received cisternal injection of saline, and untreated normal dogs, which were divided into two groups depending on the perfusion pressure during perfusion-fixation, were also examined. Microvascular corrosion casts produced by arterial injection of polyester resin were examined by scanning electron microscopy (SEM) with morphometric analysis of the caliber of the small perforating arteries. Slices sectioned parallel to the pontine surface were examined by SEM and by light microscopy with morphometric analysis of the luminal diameter and wall thickness of the small perforating arteries. Corrosion casts showed irregular width with folds in the perforating arteries 7 days after SAH. Sectioned slices showed an increased wall thickness of the perforating arteries with intimal corrugation 7 days after SAH. Morphometric analysis revealed that the extraparenchymal portion of the perforating arteries showed no significant differences between any of the groups tested; however, the intraparenchymal portion showed a significant decrease of luminal diameter 7 days after SAH, and a significant increase of wall thickness 7 and 14 days after SAH. The perfusion pressure during perfusion-fixation did not affect the histological changes in the perforating arteries. The results of this study showed that the vasoconstrictive response of the perforating arteries to SAH was different between the extraparenchymal and the intraparenchymal portion, and showed that the intraparenchymal portion of the perforating arteries constrict after SAH, which may affect cerebral ischemia during cerebral vasospasm by increasing total cerebrovascular resistance.