OBJECT: Global cerebral edema is an independent risk factor for early death and poor outcome after subarachnoid hemorrhage (SAH). In the present study, the time course of brain edema formation, neurological deficits, and neuronal cell loss were investigated in the rat filament SAH model. METHODS: Brain water content and neurological deficits were determined in rats randomized to sham (1-, 24-, or 48-hour survival), SAH by endovascular perforation (1-, 24-, or 48-hour survival), or no surgery (control). The neuronal cell count (CA1-3) was quantified in a separate set of SAH (6-, 24-, 48-, or 72-hour survival) and shamoperated animals. RESULTS: Brain water content increased significantly 24 (80.2 +/- 0.4% [SAH] vs 79.2 +/- 0.1% [sham]) and 48 hours (79.8 +/- 0.2% [SAH] vs 79.3 +/- 0.1% [sham]) after SAH. The neuroscore was significantly worse after SAH (33 +/- 15 [24 hours after SAH] vs 0 +/- 0 points [sham]) and correlated with the extent of brain edema formation (r = 0.96, p < 0.001). No hippocampal damage was present up to 72 hours after SAH. CONCLUSIONS: Brain water content and neurological dysfunction reached a maximum at 24 hours after SAH. This time point, therefore, seems to be optimal to test the effects of therapeutic interventions on brain edema formation. Neuronal cell loss was not present in CA1-3 up to 72 hours of SAH. Therefore, morphological damage needs to be evaluated at later time points.
OBJECT: Global cerebral edema is an independent risk factor for early death and poor outcome after subarachnoid hemorrhage (SAH). In the present study, the time course of brain edema formation, neurological deficits, and neuronal cell loss were investigated in the rat filament SAH model. METHODS: Brain water content and neurological deficits were determined in rats randomized to sham (1-, 24-, or 48-hour survival), SAH by endovascular perforation (1-, 24-, or 48-hour survival), or no surgery (control). The neuronal cell count (CA1-3) was quantified in a separate set of SAH (6-, 24-, 48-, or 72-hour survival) and shamoperated animals. RESULTS: Brain water content increased significantly 24 (80.2 +/- 0.4% [SAH] vs 79.2 +/- 0.1% [sham]) and 48 hours (79.8 +/- 0.2% [SAH] vs 79.3 +/- 0.1% [sham]) after SAH. The neuroscore was significantly worse after SAH (33 +/- 15 [24 hours after SAH] vs 0 +/- 0 points [sham]) and correlated with the extent of brain edema formation (r = 0.96, p < 0.001). No hippocampal damage was present up to 72 hours after SAH. CONCLUSIONS: Brain water content and neurological dysfunction reached a maximum at 24 hours after SAH. This time point, therefore, seems to be optimal to test the effects of therapeutic interventions on brain edema formation. Neuronal cell loss was not present in CA1-3 up to 72 hours of SAH. Therefore, morphological damage needs to be evaluated at later time points.
Authors: Kamil Duris; Anatol Manaenko; Hidenori Suzuki; William B Rolland; Paul R Krafft; John H Zhang Journal: Stroke Date: 2011-09-29 Impact factor: 7.914
Authors: Mutsumi Fujii; Prativa Sherchan; Paul R Krafft; William B Rolland; Yoshiteru Soejima; John H Zhang Journal: J Neurol Sci Date: 2014-04-30 Impact factor: 3.181