The effect of common carotid artery occlusion on delayed brain tissue damage in the rat double subarachnoid hemorrhage model

Abstract

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. 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. 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. CCAO leads to an aggravation of CVS-related delayed brain tissue damage in the modified rat double-SAH model.