首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Delayed cerebrovascular protective effect of lipopolysaccharide in parallel to brain ischemic tolerance.
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Delayed cerebrovascular protective effect of lipopolysaccharide in parallel to brain ischemic tolerance.

机译:脂多糖的延迟脑血管保护作用与脑缺血耐受平行。

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摘要

Cerebrovascular abnormalities, in endothelium and smooth muscle compartments, occur in the course of cerebral ischemia-reperfusion as evidenced by the impairment of endothelium-dependent relaxation and decrease in potassium inward rectifier density in occluded middle cerebral arteries (MCAs). The authors investigated whether a delayed vascular protection occurred in a model of brain ischemic tolerance. A low dose of lipopolysaccharide (0.3 mg/kg) administered 72 h before MCA occlusion induced a significant decrease in infarct volume. In parallel to this delayed neuroprotective effect, lipopolysaccharide prevented the ischemia-reperfusion-induced impairment of endothelium relaxation. In addition, lipopolysaccharide prevented the postischemic alteration of potassium inward rectifier-dependent smooth muscle relaxation as well as the decrease in potassium inward rectifier density measured by patch-clamp in dissociated vascular smooth muscle cells originated from the occluded MCA. These results suggest thatduring brain ischemic tolerance, lipopolysaccharide is able to induce both a delayed neuroprotective and vasculoprotective effect.
机译:内皮和平滑肌区室中的脑血管异常发生在脑缺血-再灌注的过程中,这由内皮依赖性舒张功能受损和闭塞的大脑中动脉(MCA)的钾内向整流因子密度降低所证明。作者研究了在脑缺血耐受模型中是否发生了延迟的血管保护。在MCA闭塞前72小时服用低剂量的脂多糖(0.3 mg / kg)可导致梗死面积明显减少。与这种延迟的神经保护作用并行的是,脂多糖阻止了缺血再灌注引起的内皮舒张损伤。此外,脂多糖可防止缺血后的钾内向整流子依赖性平滑肌松弛变化,以及通过膜片钳测定的源自闭塞性MCA的分离的血管平滑肌细胞中钾内向整流子密度的降低。这些结果表明,在脑缺血耐受期间,脂多糖能够诱导延迟的神经保护作用和血管保护作用。

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