The disparity between the decline and recovery of CPP and rCBF suggests that acute vasoconstriction occurs even in SAH of a minor extent. Acute vasoconstriction may contribute significantly to a perfusion deficit in the acute stage after SAH. The oscillating pattern of rCBF in the period of early recovery after SAH resembles the pattern of synchronized vasomotion, which has been thoroughly examined for other vascular territories and may yield therapeutic potential.

Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO 2 ) in the first 6 h after experimental SAH. Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (n = 8). Bilateral local cortical blood flow, intracranial pressure, cerebral perfusion pressure, and ptiO 2 were followed for 6 h after SAH. After induction of SAH, local cortical blood flow rapidly declined to 22% of baseline and returned to 80% after 6 h. The decline of local cortical blood flow markedly exceeded the decline of cerebral perfusion pressure. ptiO 2 declined to 57%, recovered after 2 h, and reached Z140% of baseline after 6 h. Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.

The course of cerebral blood flow after SAH resembles global ischemia followed by a continuous low-flow state caused by a sudden decrease in cerebral perfusion pressure and acute vasoconstriction. The courses of lactate and pyruvate concentrations indicate a persistently deranged aerobic metabolism.

Objective: Among various animal models of subarachnoid hemorrhage (SAH), the endovascular filament model has been found particularly suitable to investigate acute pathophysiological changes after experimental SAH. Its major drawback, however, are high mortality and high variability of results. The present studies were carried out to examine the impact of various extents of experimental SAH in rats induced by different filament sizes. Methods:In study 1, Sprague-Dawley rats were subjected to vessel perforation with a 3-0, 4-0 or 5-0 monofilament or served as controls (n = 8). Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and local cortical blood flow (LCBF) were continuously monitored for 6 hours after SAH. 24 hours later, the animals were sacrificed to evaluate subarachnoid blood effusion. In study 2, the animals were subjected to SAH using a 3-0 monofilament or served as controls (n = 8). After 7 days, they were sacrificed for quantification of tissue damage.Results: With increasing filament size, the decrease of CPP and LCBF and subarachnoid blood effusion were more pronounced. In all SAH-groups, the decline of LCBF after SAH exceeded the decline of CPP. Hippocampal damage was moderate but consistent. In both studies, the acute mortality was lower than previously reported. Conclusion:With controlled pre-hemorrhage blood pressure values and longer mechanical ventilation mortality can be kept low even if stronger filaments are used. The impact of subarachnoid vessel perforation on pathophysiological changes and blood effusion can be graded by the use of different filament sizes. The persisting mismatch between CPP and LCBF both in major and minor SAH suggests sustained vasoconstriction occurring independent of the extent of hemorrhage.

Objective: Among various animal models of subarachnoid hemorrhage (SAH), the endovascular filament model has been found particularly suitable to investigate acute pathophysiological changes after experimental SAH. Its major drawback, however, are high mortality and high variability of results. The present studies were carried out to examine the impact of various extents of experimental SAH in rats induced by different filament sizes. Methods:In study 1, Sprague-Dawley rats were subjected to vessel perforation with a 3-0, 4-0 or 5-0 monofilament or served as controls (n = 8). Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and local cortical blood flow (LCBF) were continuously monitored for 6 hours after SAH. 24 hours later, the animals were sacrificed to evaluate subarachnoid blood effusion. In study 2, the animals were subjected to SAH using a 3-0 monofilament or served as controls (n = 8). After 7 days, they were sacrificed for quantification of tissue damage.Results: With increasing filament size, the decrease of CPP and LCBF and subarachnoid blood effusion were more pronounced. In all SAH-groups, the decline of LCBF after SAH exceeded the decline of CPP. Hippocampal damage was moderate but consistent. In both studies, the acute mortality was lower than previously reported. Conclusion:With controlled pre-hemorrhage blood pressure values and longer mechanical ventilation mortality can be kept low even if stronger filaments are used. The impact of subarachnoid vessel perforation on pathophysiological changes and blood effusion can be graded by the use of different filament sizes. The persisting mismatch between CPP and LCBF both in major and minor SAH suggests sustained vasoconstriction occurring independent of the extent of hemorrhage.