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慢性高血压或蛛网膜下腔出血后血管痉挛导致脑动脉中二氧化碳诱导的扩张性丧失。

Loss of CO2-induced distensibility in cerebral arteries with chronic hypertension or vasospasm after subarachnoid hemorrhage.

作者信息

Nakajima Seiji, Kondoh Takeshi, Morishita Akitsugu, Yamashita Haruo, Kohmura Eiji, Sakurai Takashi, Yokono Koichi, Umetani Keiji

机构信息

Department of Neurosurgery, Graduate School of Medicine, Kobe University, Kobe, Japan.

出版信息

Kobe J Med Sci. 2008 Feb 8;53(6):317-26.

Abstract

We developed a rat cerebral angiography system using monochromatic synchrotron radiation X-rays at SPring-8, a third generation synchrotron radiation facility. Using new technique, we assessed the distensibility of major trunk arteries after subarachnoid hemorrhage (SAH) in normotensive and hypertensive rats. Twenty-five adult Wistar Kyoto rats (WKY) and fourteen stroke-prone spontaneously hypertensive rats (SHR) were prepared SAH by double hemorrhage injection method into cisterna magna. Angiography was performed on day 7 and was repeated three times in each rat before and after loading of hypercapnia at 100-120 mmHg of PaCO2. The diameters of major trunk vessels were assessed. Light microscopic observation of artery lumen and wall were also performed. Angiographical vasospasm was demonstrated in basilar artery in WKY with 66 % reduction in diameter of control. In ICA and other major trunk in WKY and all the arteries in SHR did not demonstrate vasospasm. SHA resulted in loss of hypercapnia-induced distention in BA of WKY. In SHR, the distensibility was impaired regardless of hemorrhage. Histological study demonstrated basilar artery in WKY thickened at 184 % after SAH and became similar to non-hemorrhagic SHR. ICA in WKY and both BA and ICA in SHR were unchanged in wall thickness before and after SAH. High quality angiography demonstrated deteriorated distensibility in chronic hypertension or SAH-induced spastic vessels.

摘要

我们利用第三代同步辐射设施——日本兵库县的SPring-8的单色同步辐射X射线,开发了一种大鼠脑血管造影系统。采用新技术,我们评估了正常血压和高血压大鼠蛛网膜下腔出血(SAH)后主要主干动脉的扩张性。将25只成年Wistar Kyoto大鼠(WKY)和14只易中风自发性高血压大鼠(SHR)通过向小脑延髓池双次注射出血法制备SAH模型。在第7天进行血管造影,并在每只大鼠吸入100 - 120 mmHg的PaCO₂ 高碳酸血症前后各重复三次。评估主要主干血管的直径。还对动脉管腔和管壁进行了光镜观察。WKY大鼠的基底动脉出现血管造影性血管痉挛,直径较对照减少66%。WKY大鼠的颈内动脉和其他主要主干以及SHR大鼠的所有动脉均未出现血管痉挛。SAH导致WKY大鼠基底动脉高碳酸血症诱导的扩张丧失。在SHR大鼠中,无论是否出血,其扩张性均受损。组织学研究表明,SAH后WKY大鼠的基底动脉增厚184%,变得与未出血的SHR大鼠相似。SAH前后,WKY大鼠的颈内动脉以及SHR大鼠的基底动脉和颈内动脉的管壁厚度均无变化。高质量的血管造影显示,慢性高血压或SAH诱导的痉挛血管的扩张性恶化。

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