首页> 外文期刊>Current Neurovascular Research >Neutralization of Interleukin-1β Reduces Vasospasm and Alters Cerebral Blood Vessel Density Following Experimental Subarachnoid Hemorrhage in Rats
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Neutralization of Interleukin-1β Reduces Vasospasm and Alters Cerebral Blood Vessel Density Following Experimental Subarachnoid Hemorrhage in Rats

机译:大鼠实验性蛛网膜下腔出血后中和白细胞介素-1β的中和作用降低了血管痉挛并改变了脑血管密度

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Subarachnoid hemorrhage (SAH) develops when extravasated arterial blood enters subarachnoid space and mixes with cerebrospinal fluid. As a result, many pathologies develop, including arterial vasospasm that leads to the ischemia and hypoxia. Immuno-inflammatory response is considered as the cause of numerous complications following SAH.nnIn the study, we examined the role of one of major cytokines, interleukin 1-beta (IL-1beta), on the vascular pathologies after experimental SAH in adult rats. SAH was produced by injection of 150 uL of autologous arterial blood into cisterna magna. In 50% of animals, IL-1beta activity was inhibited by intracerebroventricular administration of anti-rat IL-1beta antibodies (SAH' groups). Control group consisted of sham-operated rats. Ninety minutes or 24 hrs following surgery, animals were perfused transcardially and whole brains were collected. Spasm index (ratio of vessel diameter to the mean wall thickness) of basilar artery as well as blood vessel density (number of vessels per square millimeter) at brain stem and frontal part of the brain were measured. SAH led to the vasospasm of basilar artery and increased the density of blood vessel. Neutralization of IL-1beta activity significantly reduced both the vasospasm and blood vessel density only 24 hrs after SAH. The results demonstrate an important role of IL-1beta in the delayed development of vascular pathologies after subarachnoid hemorrhage.
机译:当外渗动脉血进入蛛网膜下腔并与脑脊液混合时,蛛网膜下腔出血(SAH)发生。结果,出现了许多病理,包括导致缺血和缺氧的动脉血管痉挛。免疫炎性反应被认为是SAH术后许多并发症的原因。在这项研究中,我们研究了成年大鼠实验性SAH后主要细胞因子之一白介素1-beta(IL-1beta)对血管病理的作用。通过将150 uL自体动脉血注入大水罐来生产SAH。在50%的动物中,脑室内给予抗大鼠IL-1beta抗体(SAH'组)可抑制IL-1beta活性。对照组由假手术大鼠组成。手术后90分钟或24小时,对动物进行心脏灌注,并收集全脑。测量了基底动脉的痉挛指数(血管直径与平均壁厚之比)以及脑干和大脑额叶部分的血管密度(每平方毫米的血管数)。 SAH导致基底动脉血管痉挛,并增加了血管密度。 IL-1β活性的中和作用仅在SAH后24小时显着降低了血管痉挛和血管密度。结果表明,IL-1β在蛛网膜下腔出血后血管病理的延迟发展中具有重要作用。

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