Abstract
In the intraluminal suture model of middle cerebral artery occlusion (MCAO) in the rat, lesions of the masticator muscles associated with impaired functional outcome occur. We evaluated the role of external carotid artery (ECA) transection. We assessed whether isolated interruption of an arterial or a venous connection to the ECA territory was sufficient to induce masticatory hypoperfusion and ...
Abstract
In the intraluminal suture model of middle cerebral artery occlusion (MCAO) in the rat, lesions of the masticator muscles associated with impaired functional outcome occur. We evaluated the role of external carotid artery (ECA) transection. We assessed whether isolated interruption of an arterial or a venous connection to the ECA territory was sufficient to induce masticatory hypoperfusion and lesions. We also evaluated a direct access to the common carotid artery (CCA) with subsequent vascular closure with regard to its feasibility, frequency of masticatory lesions, complications, and cerebral ischemia. Cerebral and masticatory lesions and perfusion deficits were assessed by in vivo magnetic resonance imaging (MRI). Vessel patency was evaluated using computerized tomography angiography and histology. An interruption of arterial blood flow led to masticatory hypoperfusion. Masticatory lesions occurred in 6% of the rats. Access to and closure of the CCA were feasible in all animals, leading to moderate or severe vessel stenosis in 20%, and intraarterial thrombosis in 25% of the rats. Reproducible cerebral infarctions were obtained in all animals. In 24% of the rats, hyperintense MRI signal changes were observed in the ipsilateral temporal muscle. Thus, the induction of masticatory hypoperfusion and lesions by arterial transection supports the role of the ECA in this context. Direct access to the CCA with subsequent vessel closure led to stenosis in most animals. Preservation of ECA continuity was not suitable to fully prevent masticatory lesions. (c) 2005 Elsevier Inc. All rights reserved.
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