Inapparent hemodynamic insufficiency exacerbates ischemic damage in a rat microembolic stroke model

Background and Purpose-Patients with severe carotid artery stenosis may hav e more severe ischemic damage after embolic stroke than patients without th is abnormality. Unilateral proximal carotid occlusion (UCO) alone typically does not induce infarction in normotensive rats. The aim of this study was to investigate whether UCO increases infarct size after microembolic, expe rimental stroke. Methods-Microembolic infarction was induced in 2 groups of Sprague-Dawley r ats by injecting 2000 microspheres (50-mu m diameter) intracranially from t he external carotid artery. The common carorid artery (CCA) was either liga ted just after the injection (CCA occlusion group, n = 8) or left intact (C CA open group, n = 8). In the control group (n = 4), vehicle without micros pheres was injected and the CCA was ligated. Twenty-four hours later, the b rains were removed and infarct volumes measured. Perfusion-weighted imaging was used to evaluate the cerebral circulation before and after CCA occlusi on with and without microsphere injection in a separate group of animals (n = 16). Results-All animals in the microemboli groups survived and had only a sligh t hemiparesis 24 hours after occlusion. No neurological deficits were obser ved in the control group. Infarct volumes were 145+/-57 mm(3) in the CCA oc clusion group and 45+/-26 mm(3) in the CCA open group (P < 0.01). There wer e no infarctions detected in the control group. Perfusion-weighted imaging showed that cerebral blood flow decreased after the CCA occlusion in both e xperiments with and without the microsphere injection. Conclusions-UCO alone does not induce ischemic damage, but it worsens ische mic lesion size after multiple microemboli. This is probably due to the sli ght cerebral perfusion insufficiency caused by UCO. These results suggest t hat patients with cerebral hemodynamic insufficiency, such as those with se vere carotid stenosis, may have increased ischemic damage after microemboli c events.