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Acute and Chronic Vascular Responses to Experimental Focal Arterial Stroke in the Neonate Rat

机译:对新生大鼠实验性局灶性中风的急性和慢性血管反应

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The presence of active developmental angiogenesis and vascular outgrowth in the postnatal brain may differentially affect vascular responses to stroke in newborns and adults, but very little is known about the dynamics of vascular injury and regrowth after stroke during the neonatal period. In this study, we used a clinically relevant animal model of ischemic arterial stroke in neonate rats, a transient middle cerebral artery occlusion (MCAO) in postnatal day 7, to characterize the effects of injury on vascular density and angiogenesis from acute through the chronic phase. A marked vessel degeneration and suppressed endothelial cell proliferation occur in the ischemic regions early after neonatal stroke. In contrast to what has been described in adult animals, endothelial cell proliferation and vascular density are not increased in the peri-ischemic regions during the first week after MCAO in neonates. By 2 weeks after injury, endothelial cell proliferation is increased in the cortical peri-ischemic region, but these changes are not accompanied by an increased vascular density. Suppressed angiogenesis in injured postnatal brain that we report may limit recovery after neonatal stroke. Thus, enhancement of angiogenesis after neonatal stroke may be a promising strategy for the long-term recovery of the affected newborns.
机译:产后大脑中活跃的发育性血管生成和血管增生的存在可能会不同地影响新生儿和成年人对中风的血管反应,但对新生儿期间中风后血管损伤和再生长的动态知之甚少。在这项研究中,我们使用了临床相关的新生大鼠缺血性中风的动物模型,即出生后第7天的短暂性中脑动脉闭塞(MCAO),以表征损伤对急性至慢性期对血管密度和血管生成的影响。新生儿中风后早期缺血区域出现明显的血管变性和内皮细胞增殖抑制。与成年动物所描述的相反,新生儿MCAO后的第一周,在局部缺血区域内皮细胞的增殖和血管密度并未增加。损伤后2周,皮质周围缺血区域的内皮细胞增殖增加,但这些变化并没有伴随着血管密度的增加。我们报告称,受伤的产后大脑血管生成受到抑制,这可能会限制新生儿中风后的恢复。因此,新生儿中风后血管新生的增强可能是患病新生儿长期恢复的有希望的策略。

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