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        腦干出血急性期氧化應激及炎性反應的相關性

        2019-12-02 10:30:27李肖亮陳科莫非劉傳明楊鵬
        醫(yī)學信息 2019年20期
        關鍵詞:氧化應激

        李肖亮 陳科 莫非 劉傳明 楊鵬

        摘要:目的 ?探討腦干出血急性期氧化應激和炎性反應的相關性。方法 ?收集2015年10月~2018年10月我院收治的腦干出血患者46例,依照中國腦出血診療指導規(guī)范分為死亡組(25例)和生存組(21例)。比較兩組天門冬氨酸轉氨酶(AST)、丙氨酸氨基轉移酶(ALT)、肌酐(CR)、尿素氮(BUN)、白細胞計數(WBC)、降鈣素原(PCT)、白介素6(IL-6)、血乳酸、中性粒細胞計數、鈉離子(Na)、鉀離子(K)、鈣離子(Ca)、乳酸脫氫酶(LDH)、肌酸激酶同工酶(CK-MB)、腦干出血量,分析腦干出血后氧化應激及炎性反應的相關性。結果 ?兩組CR、BUN、PCT、Na、K、Ca、LDH、CK-MB、腦干出血量比較,差異無統計學意義(P>0.05);兩組AST、ALT、WBC、中性粒細胞計數、IL-6比較,差異有統計學意義(P<0.05)。Spearman相關性分析結果顯示,WBC、中性粒細胞計數、血乳酸、IL-6、AST、ALT與腦干出血后氧化應激呈正相關(P<0.05)。多元線性Logistic回歸結果顯示,WBC、中性粒細胞計數、血乳酸水平、IL-6是腦干出血后氧化應激的獨立危險因素。結論 ?WBC、中性粒細胞計數、血乳酸水平、IL-6是腦干出血后氧化應激的獨立危險因素,可用于腦干出血急診的早期發(fā)現和干預,從而提高腦干出血急診救治成功率,進一步降低死亡率和致殘率。

        關鍵詞:腦干出血;炎性指標;氧化應激;急診救治;預后

        中圖分類號:R743.34 ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? 文獻標識碼:A ? ? ? ? ? ? ? ? ? ? ? ? ? ? ? ?DOI:10.3969/j.issn.1006-1959.2019.20.017

        文章編號:1006-1959(2019)20-0060-04

        Correlation between Oxidative Stress and Inflammatory Response in

        Acute Stage of Brain Stem Hemorrhage

        LI Xiao-liang,CHEN Ke,MO Fei,LIU Chuan-ming,YANG Peng

        Abstract:Objective ?To investigate the correlation between oxidative stress and inflammatory response in the acute phase of brain stem hemorrhage. Methods ?46 patients with brain stem hemorrhage admitted to our hospital from October 2015 to October 2018 were enrolled. According to the guidelines for diagnosis and treatment of cerebral hemorrhage in China, they were divided into death group (25 cases) and survival group (21 cases). Comparison of two groups of aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine (CR), urea nitrogen (BUN), white blood cell count (WBC), procalcitonin (PCT), interleukin 6 ( IL-6), blood lactate, neutrophil count, sodium ion (Na), potassium ion (K), calcium ion (Ca), lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB ), the amount of brain stem bleeding, analysis of the correlation between oxidative stress and inflammatory response after brain stem hemorrhage. Results ?There were no significant differences in CR, BUN, PCT, Na, K, Ca, LDH, CK-MB, and brain stem bleeding between the two groups (P>0.05). AST, ALT, WBC, and neutrophil counts in the two groups. Compared with IL-6, the difference was statistically significant (P<0.05). Spearman correlation analysis showed that WBC, neutrophil count, blood lactate, IL-6, AST, ALT were positively correlated with oxidative stress after brain stem hemorrhage (P<0.05). Multivariate linear logistic regression showed that WBC, neutrophil count, blood lactate level, and IL-6 were independent risk factors for oxidative stress after brain stem hemorrhage.Conclusion ?WBC, neutrophil count, blood lactate level and IL-6 are independent risk factors for oxidative stress after brain stem hemorrhage. They can be used for early detection and intervention of emergency treatment of brain stem hemorrhage, thus improving the success rate of emergency treatment of brain stem hemorrhage. To further reduce mortality and disability.

        腦出血后血腫周圍區(qū)域存有大量浸潤性巨噬細胞,增加心臟和血清中ICAM-1、MCP-1、IL-1的表達,同時增加了腦出血后炎癥細胞(白細胞和巨噬細胞)向心臟的浸潤,增加心臟組織炎癥因子的表達,但腦干出血相關炎性反應報道甚少[12]。Wei L等[13]對腦出血后小鼠的腦-心相互作用研究發(fā)現,來自受損心肌的炎癥因子與腦組織產生的炎癥因子有協同作用,在小鼠沒有原發(fā)性心臟病的情況下,腦出血增加了心臟組織中心臟氧化應激和炎癥因子的表達,誘導小鼠出現明顯的進行性心功能障礙,并伴有心臟纖維化、心肌細胞肥大和凋亡的增加,證明腦出血可誘導進行性心臟缺血。Okamoto K等[14]報道1例長期反復腦出血患者腦橋和中腦內可見大量AT8免疫反應神經元和突起,提示氧化應激可能加速腦干磷酸化tau蛋白的積累。

        本研究中兩組AST、ALT比較,差異有統計學意義(P<0.05),說明神經系統和免疫系統相互影響,但腦干出血患者心肌損傷表現(LDH、CK-MB)未見明顯差異,可能與腦干出血早期/超早期氧化應激損傷尚未波及心血管系統有關,相關機制尚待進一步研究。

        綜上所述,WBC、中性粒細胞計數、血乳酸水平、IL-6是腦干出血后氧化應激的獨立危險因素,可用于腦干出血急診的早期發(fā)現和干預,從而提高腦干出血急診救治成功率,進一步降低死亡率和致殘率。

        參考文獻:

        [1]楊樹源,張建寧.神經外科學[M].北京:人民衛(wèi)生出版社,2015.

        [2]中華醫(yī)學會神經病學分會.中國腦出血診治指南[J].中華神經科雜志,2015,48(6):435-444.

        [3]Murakami M,Fujioka S,Oyama T,et al.Serial changes in the regional cerebral blood flow of patients with hypertensive intracerebral hemorrhage:long-term follow-up SPECT study[J].J Neurosurg Sci,2015,49(3):117-124.

        [4]Ordónez-Rubiano EG,Johnson JM,Younus I,et al.Recovery of consciousness after a brainstem cavernous malformation hemorrhage:A descriptive study of preserved reticular activating system with tractography[J].Journal of Clinical Neuroscience,2019(59):372-377.

        [5]Lekic T,Rolland W,Manaenko A,et al.Evaluation of the hematoma consequences,neurobehavioral profiles,and histopathology in a rat model of pontine hemorrhage[J].J Neurosurg,2013,118(2):465-477.

        [6]李敬,李穎,郭麗娟,等.腦干出血并發(fā)腦心綜合征心律失常與兒茶酚胺濃度的臨床分析[J].中國現代醫(yī)學雜志,2016,26(23):59-62.

        [7]Schneider U,Davids A,Brandenburg S,et al.Microglia inflict delayed brain injury after subarachnoid hemorrhage[J].Acta Neuropathol,2015,130(2):215-231.

        [8]Wakai T,Sakata H,Narasimhan P,et al.Transplantation of neural stem cells that overexpress SOD1 enhances amelioration of intracerebral hemorrhage in mice[J].J Cereb Blood Flow Metab,2014,34(3):203-215.

        [9]Mewhort HE,Lipon BD,Svystonyuk DA,et al.Monocytes increase human cardiac myofibroblast-mediated extracellular matrix remodeling through TGF-beta1[J].Am J Physiol Heart Circ Physiol,2016(310):716-724.

        [10]Zhou F,Jiang Z,Yang B,et al.Magnolol exhibits anti-inflammatory and neuroprotective effects in a rat model of intracerebral haemorrhage[J].Brain Behav Immun,2018(12):28.

        [11]Erdi F,Keskin F,Esen H,et al.Telmisartan ameliorates oxidative stress and subarachnoid haemorrhage-induced cerebral vasospasm[J].Neurol Res,2016,38(3)626-641.

        [12]Lin L,Yihao T,Zhou F,et al.Inflammatory regulation by driving microglial M2 polarization:neuroprotective effects of cannabinoid receptor-2 activation in intracerebral hemorrhage[J].Front Immunol,2017(8):112-119.

        [13]Wei L,Lilin L,Michael C,et al.Intracerebral Hemorrhage Induces Cardiac Dysfunction in Mice Without Primary Cardiac Disease[J].Front Neurol,2018(9):965-973.

        [14]Okamoto K,Naito I,Fukuda T,et al.Adult moyamoya disease associated with abundant phosphorylated tau accumulation in the brainstem:Report of a case with autopsy findings[J].Neuropathology,2018,38(3):224.

        收稿日期:2019-5-6;修回日期:2019-6-10

        編輯/杜帆

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