OBJECTIVE: Delayed ischemic brain tissue damage in the time course of cerebral vasospasm in the rat double-subarachnoid hemorrhage (SAH) model has been described before. However, in order to enhance hemodynamic insufficiency during cerebral vasospasm (CVS), we performed-in a modification to the standard double-hemorrhage model-an additional unilateral common carotid artery occlusion (CCAO), expecting aggravation of brain-tissue damage in areas particularly sensitive to hypoxia. METHODS: CVS was induced by injection of 0.25 ml autologous blood twice in the cisterna magna of Sprague-Dawley rats with and without unilateral CCAO. The animals were examined on days 2, 3, 4 and 5, and compared with the sham-operated control group without SAH. The functional deficits were graded between 0 and 3. Perfusion weighted imaging (PWI) at 3 Tesla magnetic resonance (MR) tomography was performed to assess cerebral blood flow (CBF). The brains were fixed, stained and evaluated for histological changes. RESULTS: On day 5, the neurological state was significantly worse in rats with SAH. The relative CBF/muscle blood ratio was significantly decreased by SAH and lowest in rats with CCAO and SAH (4.5 ± 1.1 vs 2.7 ± 0.6) compared with sham (7.9 ± 1.5; p < 0.001). Basilar artery (BA) diameter was 79 ± 5 μm (SAH) vs 147 ± 4 μm (sham, p < 0.001). Neuronal cell count in the hippocampal areas CA1-CA4 was significantly reduced by SAH on day 5 (p < 0.001) and lowest in rats with SAH and CCAO. CONCLUSIONS: CCAO leads to an aggravation of CVS-related delayed brain tissue damage in the modified rat double-SAH model.
OBJECTIVE: Delayed ischemic brain tissue damage in the time course of cerebral vasospasm in the rat double-subarachnoid hemorrhage (SAH) model has been described before. However, in order to enhance hemodynamic insufficiency during cerebral vasospasm (CVS), we performed-in a modification to the standard double-hemorrhage model-an additional unilateral common carotid artery occlusion (CCAO), expecting aggravation of brain-tissue damage in areas particularly sensitive to hypoxia. METHODS: CVS was induced by injection of 0.25 ml autologous blood twice in the cisterna magna of Sprague-Dawley rats with and without unilateral CCAO. The animals were examined on days 2, 3, 4 and 5, and compared with the sham-operated control group without SAH. The functional deficits were graded between 0 and 3. Perfusion weighted imaging (PWI) at 3 Tesla magnetic resonance (MR) tomography was performed to assess cerebral blood flow (CBF). The brains were fixed, stained and evaluated for histological changes. RESULTS: On day 5, the neurological state was significantly worse in rats with SAH. The relative CBF/muscle blood ratio was significantly decreased by SAH and lowest in rats with CCAO and SAH (4.5 ± 1.1 vs 2.7 ± 0.6) compared with sham (7.9 ± 1.5; p < 0.001). Basilar artery (BA) diameter was 79 ± 5 μm (SAH) vs 147 ± 4 μm (sham, p < 0.001). Neuronal cell count in the hippocampal areas CA1-CA4 was significantly reduced by SAH on day 5 (p < 0.001) and lowest in rats with SAH and CCAO. CONCLUSIONS:CCAO leads to an aggravation of CVS-related delayed brain tissue damage in the modified rat double-SAH model.
Authors: Ari Dienel; Remya Ammassam Veettil; Sung-Ha Hong; Kanako Matsumura; Peeyush Kumar T; Yuanqing Yan; Spiros L Blackburn; Leomar Y Ballester; Sean P Marrelli; Louise D McCullough; Devin W McBride Journal: Stroke Date: 2020-06-16 Impact factor: 7.914
Authors: Jenna L Leclerc; Joshua M Garcia; Matthew A Diller; Anne-Marie Carpenter; Pradip K Kamat; Brian L Hoh; Sylvain Doré Journal: Front Mol Neurosci Date: 2018-03-22 Impact factor: 5.639