Abstract
The effects of early relief of heavy bilateral carotid stenosis and ischemic postconditioning on hippocampus CA1 neurons are still unclear. In this study, we used a rat model to imitate severe bilateral carotid stenosis in humans. The rats were divided into sham group, carotid stenosis group, stenosis relief group and ischemic postconditioning group. Ischemic postconditioning consisted of three cycles of 30 s ischemia and 30 s reperfusion. The cerebral blood flow was measured with a laser Doppler flowmeter. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and the number of live neurons was assessed by cell counting under a light microscope. The levels of oxidative products MDA and 8-iso-PGF2α, inflammatory factors IL-1β and TNF-α, and the activities of anti-oxidative enzymes SOD and CAT were assayed by specific enzyme-linked immunosorbent assay (ELISA) kits, respectively. We found that relief of carotid stenosis and ischemic postconditioning could increase cerebral blood flow. When stenosis was relieved, the percentage of live neurons was 66.6% ± 6.2% on day 3 and 62.3% ± 9.8% on day 27, which was significantly higher than 55.5% ± 4.8% in stenosis group. Ischemic postconditioning markedly improved the live neurons to 92.5% ± 6.7% on day 3 and 88.6% ± 9.1% on day 27. Further study showed that, neuronal death caused by relief of stenosis is associated with increased oxidative stress and enhanced inflammatory response, and the protection of ischemic postconditioning is related to inhibition of oxidative stress and suppression of inflammatory response.
Highlights
Carotid artery stenosis remains a major public health issue in the developed countries [1]
Between the two groups treated with and without ischemic postconditioning. These results indicated that relief of carotid stenosis could increase cerebral blood flow (CBF), but no significant changes could be found in CBF
We found that three cycles of 30 s ischemia and 30 s reperfusion administrated prior to re-establishment of cerebral blood supply significantly protected neuronal injury due to relief of carotid stenosis, and made the percentage of live neurons improve to 92.5% ± 6.7% on day 3 (p < 0.01 vs. stenosis relief group) and 88.6% ± 9.1% on day 27 (p < 0.01 vs. stenosis relief group), respectively
Summary
Carotid artery stenosis remains a major public health issue in the developed countries [1]. Clinical studies have shown that patients with carotid stenosis would have cognition dysfunction due to long-term cerebral hypoperfusion [3,4]. Animal study demonstrated that almost 50% of the neurons in rat hippocampus CA1 region would die at 30 days when severe bilateral carotid artery stenosis was produced [5]. Revascularization of the stenotic artery has become the first choice of treatment for the patients with severe carotid stenosis [8]. Recent clinical report showed that early revascularization within 7 days can be safely performed and is preferred over delaying operative treatment in the symptomatic carotid stenosis patients without evidence of intracerebral hemorrhage, carotid occlusion, or permanent neurologic deficits [10]. We speculate that early relief of carotid stenosis would benefit hippocampus CA1 neurons which are responsible for cognitive function. In this study, we used rat to establish the model of severe carotid stenosis and investigated the effects of early relief of carotid stenosis on CA1 neurons that are vulnerable to reperfusion
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