Evidence was found for different outcomes to middle cerebral artery occlusion in the young genetically hypertensive stroke-prone rat (SHRSP) compared to sham operated controls and the Wistar Kyoto rat (WKY). Qualitatively and quantitatively different gross lesions marked by Evans blue-albumin, cortical atrophy, large areas of strikingly altered cortical histology, postoperative survival and motor behavioral deficits differentiate young SHRSP from sham operated controls and the normotensive WKY. We conclude that the limited focal lesion observed in normotensive and sham operated rats is primarily due to surgical trauma of exposing the vessel and passing the ligature deep to it. The grossly larger and qualitatively different lesion in the SHRSP is the result of an inadequate circulation provided by the dorsal cerebral arterial collaterals. Since the 5–6 week old SHRSP were only mildly hypertensive (systolic blood pressure 140 mm Hg), the inadequate collateral circulation appears to be related to either a genetic or acquired problem rather than being secondary to a vascular lesion of chronic hypertension.