Ewelina Grzywna, Krzysztof Stachura, Marek Moskala, Krzysztof Kruczala
Department of Neurosurgery and Neurotraumatology, Jagiellonian University Medical College, Krakow, Poland.
Faculty of Chemistry, Jagiellonian University, Krakow, Poland.
Cell Biochem Biophys. 2017 Dec;75(3-4):351-358. doi: 10.1007/s12013-017-0820-7. Epub 2017 Sep 25.
Pathophysiology of delayed cerebral ischemia and cerebral vasospasm following aneurysmal subarachnoid hemorrhage is still poorly recognized, however free radicals are postulated as one of the crucial players. This study was designed to scrutinize whether the concentration of free radicals in the peripheral venous blood is related to the occurrence of delayed cerebral ischemia associated with cerebral vasospasm. Twenty-four aneurysmal subarachnoid hemorrhage patients and seven patients with unruptured intracranial aneurysm (control group) have been studied. Free radicals in patients' blood have been detected by the electron paramagnetic resonance (CMH.HCl spin probe, 150 K, ELEXSYS E500 spectrometer) on admission and at least 72 h from disease onset. Delayed cerebral ischemia monitoring was performed by daily neurological follow-up and transcranial color coded Doppler. Delayed cerebral ischemia observed in six aneurysmal subarachnoid hemorrhage patients was accompanied by cerebral vasospasm in all six cases. No statistically significant difference in average free radicals concentration between controls and study subgroups was noticed on admission (p = .3; Kruskal-Wallis test). After 72 h free radicals concentration in delayed cerebral ischemia patients (3.19 ± 1.52 mmol/l) differed significantly from the concentration in aneurysmal subarachnoid hemorrhage patients without delayed cerebral ischemia (0.65 ± 0.37 mmol/l) (p = .012; Mann-Whitney test). These findings are consistent with our assumptions and seem to confirm the role of free radicals in delayed cerebral ischemia development. Preliminary results presented above are promising and we need perform further investigation to establish whether blood free radicals concentration may serve as the biomarker of delayed cerebral ischemia associated with cerebral vasospasm.
动脉瘤性蛛网膜下腔出血后迟发性脑缺血和脑血管痉挛的病理生理学仍未得到充分认识,然而自由基被认为是关键因素之一。本研究旨在探讨外周静脉血中自由基浓度是否与伴有脑血管痉挛的迟发性脑缺血的发生有关。研究了24例动脉瘤性蛛网膜下腔出血患者和7例未破裂颅内动脉瘤患者(对照组)。在入院时以及发病至少72小时后,通过电子顺磁共振(CMH.HCl自旋探针,150K,ELEXSYS E500光谱仪)检测患者血液中的自由基。通过每日神经学随访和经颅彩色编码多普勒进行迟发性脑缺血监测。在6例动脉瘤性蛛网膜下腔出血患者中观察到的迟发性脑缺血,所有6例均伴有脑血管痉挛。入院时,对照组与研究亚组之间的平均自由基浓度无统计学显著差异(p = 0.3;Kruskal-Wallis检验)。72小时后,迟发性脑缺血患者的自由基浓度(3.19±1.52 mmol/l)与无迟发性脑缺血的动脉瘤性蛛网膜下腔出血患者的浓度(0.65±0.37 mmol/l)有显著差异(p = 0.012;Mann-Whitney检验)。这些发现与我们的假设一致,似乎证实了自由基在迟发性脑缺血发展中的作用。上述初步结果很有前景,我们需要进一步研究以确定血液自由基浓度是否可作为伴有脑血管痉挛的迟发性脑缺血的生物标志物。