Impact of various extents of experimental subarachnoid hemorrhage induced by the endovascular filament model on mortality and changes of cerebral blood flow

Abstract

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.

Analysis of cerebral glucose metabolism following experimental subarachnoid hemorrhage over 7 days

“…Although there might be a bias via the usage of anesthetics such as isoflurane 38 , this experiment would not be possible without anesthesia. The mortality rate of SAH animals would drastically increase without sedation and intubation because of the sharp initial increase of intracranial pressure (ICP) immediately after SAH and the possible consecutive breathing arrest 39 . In addition, PET-scans in SAH rats would not be possible without anesthesia or only with results of enormous blurring.…”

Magnesium treatment for neuroprotection in ischemic diseases of the brain

“…Starting immediately after SAH, a dissociation of cerebral perfusion pressure and CBF has been found which enhances and prolongs the early perfusion deficit after SAH. It is likely to be caused by an acute vasoconstriction, a disseminated cerebrovascular reaction [46,47]. Finally, delayed vasospasm of subarachnoid vessels appears in a high percentage of SAH patients within the first 2 weeks after SAH.…”