Liu Zun-Wei, Gu Hua, Zhang Bin-Fei, Zhao Ya-Hui, Zhao Jun-Jie, Zhao Yong-Lin, Ma Xu-Dong, Song Jin-Ning
Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, Shaanxi 710061, People׳s Republic of China.
Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, Shaanxi 710061, People׳s Republic of China; Department of Orthopedic trauma, Honghui Hospital, Xi'an Jiaotong University Health Science Center, No. 76 Nanguo Road, Xi'an, Shaanxi 710061, People׳s Republic of China.
Brain Res. 2016 May 15;1639:108-19. doi: 10.1016/j.brainres.2016.02.038. Epub 2016 Mar 2.
To investigate the dynamic expression of vasopressin and its potential role in rat brain tissue after experimental subarachnoid hemorrhage (SAH).
Male Sprague-Dawley rats were divided into 10min, 1h, 6h, 24h, 48h and 72h groups. The SAH model was established by endovascular puncture. ELISA and immunohistochemistry were performed to evaluate dynamic expression of vasopressin. Immunohistochemistry of GPIIb/IIIa integrin was used to assess platelet aggregation. Double immunofluorescence labeling was carried out to observe the reaction between vasopressin and platelet. Early brain injury was evaluated by apoptotic cells counting. Neurobehavioral score was performed to assess neuroprotective role of SR 49059 (a selective antagonists of vasopressin receptor).
In peripheral blood and hypothalamus, vasopressin increased rapidly at 6h and 24h. Expression of GPIIb/IIIa integrin peaked at 24h in cortex and hippocampus. Immunofluorescence showed that vasopressin and GPIIb/IIIa integrin located at the same site. Administration of SR 49059 significantly decreased platelet aggregation and number of apoptotic cells. The neurobehavioral score was promoted significantly after the intervention.
The results indicate that rapidly increased vasopressin could induce platelet aggregation and contribute to early brain injury after SAH.
研究实验性蛛网膜下腔出血（SAH）后大鼠脑组织中血管加压素的动态表达及其潜在作用。
将雄性Sprague-Dawley大鼠分为10分钟、1小时、6小时、24小时、48小时和72小时组。通过血管内穿刺建立SAH模型。采用酶联免疫吸附测定（ELISA）和免疫组织化学法评估血管加压素的动态表达。采用GPIIb/IIIa整合素免疫组织化学法评估血小板聚集情况。进行双重免疫荧光标记以观察血管加压素与血小板之间的反应。通过凋亡细胞计数评估早期脑损伤。进行神经行为评分以评估SR 49059（一种血管加压素受体选择性拮抗剂）的神经保护作用。
在外周血和下丘脑中，血管加压素在6小时和24小时迅速升高。皮质和海马中GPIIb/IIIa整合素的表达在24小时达到峰值。免疫荧光显示血管加压素和GPIIb/IIIa整合素位于同一部位。给予SR 49059可显著降低血小板聚集和凋亡细胞数量。干预后神经行为评分显著提高。
结果表明，血管加压素的迅速升高可诱导血小板聚集，并导致SAH后早期脑损伤。
