Chakhoyan Ararat, Corroyer-Dulmont Aurélien, Leblond Marine M, Gérault Aurélie, Toutain Jérôme, Chazaviel Laurent, Divoux Didier, Petit Edwige, MacKenzie Eric T, Kauffmann François, Delcroix Nicolas, Bernaudin Myriam, Touzani Omar, Valable Samuel
1 CNRS, UMR6301-ISTCT, CERVOxy Group, GIP CYCERON, Caen, France.
2 CEA, DSV/I2BM, GIP CYCERON, Caen, France.
J Cereb Blood Flow Metab. 2017 Jun;37(6):2270-2282. doi: 10.1177/0271678X16663947. Epub 2016 Jan 1.
The alleviation of hypoxia in glioblastoma with carbogen to improve treatment has met with limited success. Our hypothesis is that the eventual benefits of carbogen depend on the capacity for vasodilation. We examined, with MRI, changes in fractional cerebral blood volume, blood oxygen saturation, and blood oxygenation level dependent signals in response to carbogen. The analyses were performed in two xenograft models of glioma (U87 and U251) recognized to have different vascular patterns. Carbogen increased fractional cerebral blood volume, blood oxygen saturation, and blood oxygenation level dependent signals in contralateral tissues. In the tumor core and peritumoral regions, changes were dependent on the capacity to vasodilate rather than on resting fractional cerebral blood volume. In the highly vascularised U87 tumor, carbogen induced a greater increase in fractional cerebral blood volume and blood oxygen saturation in comparison to the less vascularized U251 tumor. The blood oxygenation level dependent signal revealed a delayed response in U251 tumors relative to the contralateral tissue. Additionally, we highlight the considerable heterogeneity of fractional cerebral blood volume, blood oxygen saturation, and blood oxygenation level dependent within U251 tumor in which multiple compartments co-exist (tumor core, rim and peritumoral regions). Finally, our study underlines the complexity of the flow/metabolism interactions in different models of glioblastoma. These irregularities should be taken into account in order to palliate intratumoral hypoxia in clinical trials.
用卡波金缓解胶质母细胞瘤中的缺氧以改善治疗的效果有限。我们的假设是卡波金的最终益处取决于血管舒张能力。我们通过磁共振成像(MRI)检查了脑血容量分数、血氧饱和度和血氧水平依赖信号在给予卡波金后的变化。分析在两种公认具有不同血管模式的胶质瘤异种移植模型(U87和U251)中进行。卡波金增加了对侧组织中的脑血容量分数、血氧饱和度和血氧水平依赖信号。在肿瘤核心和瘤周区域,变化取决于血管舒张能力而非静息脑血容量分数。与血管化程度较低的U251肿瘤相比,在血管化程度高的U87肿瘤中,卡波金诱导脑血容量分数和血氧饱和度有更大增加。血氧水平依赖信号显示U251肿瘤相对于对侧组织有延迟反应。此外,我们强调了U251肿瘤内脑血容量分数、血氧饱和度和血氧水平依赖存在相当大的异质性,其中多个区域共存(肿瘤核心、边缘和瘤周区域)。最后,我们的研究强调了不同胶质母细胞瘤模型中血流/代谢相互作用的复杂性。在临床试验中缓解肿瘤内缺氧时应考虑这些不规则性。