Vascularization pattern after ischemic stroke is different in control versus diabetic rats: relevance to stroke recovery.
Vascularization pattern after ischemic stroke is different in control versus diabetic rats: relevance to stroke recovery.
复制标题
缺血性中风后的血管化模式在对照中与糖尿病大鼠相关：与中风恢复相关。
DOI：
10.1161/strokeaha.113.001660
复制
发表时间：
2013-10
期刊：
影响因子：
8.3
通讯作者：
Ergul A
中科院分区：
文献类型：
--
作者：
Prakash R;Li W;Qu Z;Johnson MA;Fagan SC;Ergul A
先前存在的糖尿病会使缺血性中风的大脑功能恶化。我们之前已经表明，2 型糖尿病大鼠表现出功能失调性脑新生血管形成增强，当这些大鼠遭受脑缺血再灌注损伤时，会发生出血性转化 (HT) 和更大的神经功能缺损。然而，我们对糖尿病中风恢复阶段血管和功能可塑性的了解有限。这项研究检验了糖尿病中风后血管修复受损的假设，这与感觉运动和认知功能较差有关。我们进一步假设血糖控制可以防止血管化受损并改善糖尿病的功能结果。缺血再灌注损伤后 14 天，对对照组、糖尿病组和糖尿病加二甲双胍组以及各自的假对照组的同侧和对侧半球的血管化进行评估。通过共聚焦显微镜实现 FITC 染色脉管系统的 3 维重建，并测量包括血管体积和表面积在内的体视学参数。通过 GFAP 染色测定星形胶质细胞增生。评估了感觉运动恢复、认知能力下降和自发活动的相对率。糖尿病大鼠梗塞周围区域的血管密度显着降低，而对照大鼠则出现修复性新血管形成。与对照中风相比，糖尿病中风的星形胶质细胞肿胀和反应性更明显。糖尿病会削弱感觉运动的恢复，还会加剧焦虑样症状和认知缺陷。中风后开始的血糖控制部分阻止了这些变化。糖尿病会损害中风后修复性新血管形成并阻碍康复。中风后的血糖控制可以改善神经血管修复并改善功能结果。
Pre-existing diabetes worsens brain functionality in ischemic stroke. We have previously shown that type-2-diabetic rats exhibit enhanced dysfunctional cerebral neovascularization and when these rats are subjected to cerebral ischemic reperfusion injury develop hemorrhagic transformation (HT) and greater neurological deficits. However, our knowledge of vascular and functional plasticity during the recovery phase of diabetic stroke is limited. This study tested the hypothesis that vascular repair is impaired in the post-stroke period in diabetes, and this is associated with poor sensorimotor and cognitive function. We further hypothesized that glycemic control prevents impaired vascularization and improves functional outcome in diabetes. Vascularization was assessed in the ipsilateral and contralateral hemispheres in control, diabetes and diabetes plus metformin groups 14 days after ischemic reperfusion injury as well as in respective sham controls. 3-dimensional reconstruction of the FITC stained vasculature was achieved by confocal microscopy and stereological parameters including vascular volume and surface area were measured. Astrogliosis was determined by GFAP staining. The relative rates of sensorimotor recovery, cognitive decline and spontaneous activity were assessed. Vascular density in the peri-infarct area was significantly reduced in diabetes whereas there was reparative neovascularization in control rats. Astroglial swelling and reactivity was more pronounced in diabetic stroke compared to control stroke. Diabetes blunted sensorimotor recovery and also exacerbated anxiety-like symptoms and cognitive deficits. Glycemic control started after stroke partially prevented these changes. Diabetes impairs post-stroke reparative neovascularization and impedes the recovery. Glycemic control after stroke can improve neurovascular repair and improve functional outcome.