The pathophysiological changes following aneurysmal subarachnoid hemorrhage (SAH) are commonly divided into early consequences (developing shortly after the bleeding) and delayed consequences of the bleeding. The development of delayed injury mechanisms, e.g., reduced cerebral blood flow (CBF) caused by cerebral vasospasm (CVS) or development of delayed ischemic neurological deficits (DIND), seem mainly to depend on the amount and duration of the subarachnoid blood clot. CVS may progress to cerebral ischemia and infarction, and therefore lead to delayed neurological deterioration. The rat double-hemorrhage model reproduces the time course of the delayed pathophysiological consequences of CVS, which imitates the clinical setting more precisely than other rodent models. Furthermore, this model is adjustable via various technical considerations or modifications. Therefore, the double-hemorrhage model is predisposed to be used to mimic the delayed effects of SAH and to investigate the use of drugs on morphological ischemic, functional, and vasospastic effects.