Brain edema formation correlates with perfusion deficit during the first six hours after experimental subarachnoid hemorrhage in rats

Male Sprague–Dawley rats, randomly assigned to one of six groups (n = 8), were subjected to SAH using the endovascular filament model or underwent a sham operation. Animals were sacrificed 15, 30, 60, 180 or 360 minutes after SAH. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and bilateral local cerebral blood flow (LCBF) were continuously measured. Brain water content (BWC) was determined by the wet/dry-weight method.After SAH, CPP and LCBF rapidly decreased. The decline of LCBF markedly exceeded the decline of CPP and persisted until the end of the observation period. BWC continuously increased. A significant correlation was observed between the BWC and the extent of the perfusion deficit in animals sacrificed after 180 and 360 minutes.The significant correlation with the perfusion deficit after SAH suggests that the development of brain edema is related to the extent of ischemia and acute vasoconstriction in the first hours after SAH.Severe brain edema is observed in a number of patients after aneurysmal subarachnoid hemorrhage (SAH) and occurs irrespective of vasospasm-related territorial infarction. Global brain swelling is observed in 20% of SAH patients and is an independent risk factor for poor outcome [1]. However, information about the pathogenesis and the time-course of brain edema in the first hours after SAH is scarce. To date, experimental studies on the development of brain edema after SAH have covered the first 2 – 3 days after induction of hemorrhage. However, the course of brain edema in the first hours after SAH has not been investigated yet [2,3], although information about a possible treatment and its timing might be derived from this data. This study was conducted to examine the development of brain swelling and its correlation to hemodynamic and perfusion parameters in the first six hours after experimental SAH in rats.For the experiments, 48 male Sprague–Dawley rats weighing 250–300 g were